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Events

Sep

20

Stem Cells & Regenerative Biology Seminar Series

Chicago - 12:00 PM - 1:00 PM

Presented By: Christopher Glass, MD, PhDDistinguished Professor of Cellular and Molecular MedicineBen and Wanda Hildyard Chair in Hereditary DiseasesSchool of MedicineUniversity of California, San Diego

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Sep

23

Pharmacologic Tools Probe Mitochondrial Behavior in Health and Disease

Chicago - 4:00 PM - 5:00 PM

Madesh Muniswamy, Ph.D.Professor of NephrologyUniversity of Texas - San Antonio The Muniswamy laboratory currently explores cutting-edge optical imaging-based methods to address major questions pertaining to explore the phenomenon referred as mitochondrial shape transition (MIST), a process that is independent of fission or fusion (Cell Reports 2018). With these observations, we currently are employing new pharmacologic tools to probe organellar communication and cell function. Our hope is to offer deeper insights behind inter-organellar communication that might be exploited to precisely treat various forms of disease.

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Sep

25

BMG Guest Seminar Speaker: Judd F. Hultquist, PhD

Chicago - 10:00 AM - 11:00 AM

The Department of Biochemistry and Molecular Genetics presents: Judd F Hultquist, PhDAssistant Professor of Medicine (Infectious Diseases)Robert H. Lurie Medical Research Center  

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Sep

26

BMG Seminar: Decoding the cancer genome one codon at a time and its therapeutic implications -Davide Ruggero, PhD

Chicago - 10:00 AM - 11:00 AM

Our research is centered on understanding translational control of gene expression in both normal health and disease, with a particular focus on cancer biology. Our research combines mouse genetics with genome-wide translational profiling, in-depth molecular biology, and pharmacology to systematically define the points of regulation, in cis and trans, by which the genome is selectively decoded into proteins in a cell- and tissue-specific manner. We have uncovered that a common denominator of multiple oncogenic pathways is their ability to directly control the core translation machinery of a cell, resulting in the rapid remodeling of mRNA translation programs that promote distinct hallmarks of cancer development, such as cell growth, metabolism, and increased motility. Our most recent findings delineate the in vivo requirements for a distinct threshold of the major cap-binding protein, eIF4E, in normal organismal development compared to those required for translating the cancer genome. We show that increased eIF4E activity is essential for cancer cell survival as distinct subsets of mRNAs that regulate the cancer cell oxidative response are marked by the presence of a novel, eIF4E-dependent cis-acting motif present in their 5’UTRs. I will also discuss a new link between translational nutrient availability to maintain metabolic fitness and health span in vivo. In particular, we are defining the role of translation regulation for the first time in the poorly understood molecular program underlying increased risk of cancer development associated with obesity. I will also discuss the generation of the first comprehensive systems-level analysis of the ‘cancer translatome’ during cancer development in vivo that highlights a dichotomy in transcriptional vs. translational control of gene expression guiding key, select steps in cancer development and evolution. The immediate impact of our research has been the design of a new generation of compounds to target the aberrant translation machinery in cancer cells, which are currently in clinical trials, and may reflect a new frontier in cancer therapy. Davide Ruggero, PhDProfessor, Department of UrologyHelen Diller Family Chair in Basic Cancer ResearchUniversity of California San Francisco  

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Sep

26

Genetics and Biology of the Human Circadian System - Louis Ptáček, MD

Chicago - 2:00 PM - 3:00 PM

Join us remotely via BlueJeans.  The Center for Autism and Neurodevelopment of Northwestern University Feinberg School of Medicine welcomes you to attend a lecture featuring: Louis Ptáček, MDJohn C. Coleman Distinguished Professor of NeurologyUniversity of California, San Francisco Sleep contributes to our physical and mental health, and sleep perturbation has been linked to many health conditions. However, understanding of the human circadian system was impossible until the recognition of extreme behavioral variants of the human circadian system. The Mendelian trait of familial advanced sleep phase (FASP) 20 years ago opened up the possibility of identifying human genes and mutations that regulate the human clock. We have been studying many FASP families to identify such genetic variant and to probe the in vitro and in vivo functional consequences of such variants. These studies have led to many novel insights into the human circadian clock. Our work over the last 20 years has now culminated with reported estimates of FASP prevalence that is much higher than anyone could have predicted before. The resource of human families is leading to identification of novel circadian genes. Dr. Louis Ptáček has used the tools of human genetics in the study of patients with an impressive range of human phenotypes. He pioneered the field of “Channelopathies” which encompasses a large group of episodic/electrical disorders of muscle, heart, and brain. His earliest work focused a group of rare episodic muscle diseases he had proposed as models for more complex episodic/electrical disorders like cardiac arrhythmias and epilepsy. In an elegant set of papers, he systematically cloned and characterized all the genes causing a variety of familial periodic paralyses. All encode ion channels and work from his and other labs has shown that homologs of these are the cause of some forms of cardiac arrhythmias, epilepsy, and migraine headache. Subsequently, his group has done extensive work in characterizing the functional consequences of disease causing mutations.To this point, Ptáček’s work had focused on human diseases. In another line of work motivated by a family with an interesting phenotype, he has now embarked into the challenging field of behavioral genetics. He and his colleague, Ying-Hui Fu, study the genetics of human sleep phenotypes. Familial advanced sleep phase (FASP), is manifest as a lifelong trait of extremely early sleep times and early morning awakening (1 am – 4 am). Ptáček and Fu have gone on to characterize mutations in a growing list of genes that underlie the phenotype in ~15% of FASP families. Furthermore, they’ve gone on to model human mutations in Drosophila and mice. In vitro and in vivo experiments focused on regions harboring the human mutations has led to novel insights in fine tuning of circadian period regulation by phosphorylation and other post translational modifications.He serves on a number editorial boards including Neurogenetics, eLife, and the Journal of Clinical Investigation. He is a member of the National Academy of Medicine, the American Association of Arts and Sciences, and the National Academy of Science.

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Sep

27

"Targeting Stem Cells for Neurodevelopmental Disorders"

Chicago - 12:00 PM - 1:00 PM

The department of Physiology welcomes Xinyu Zhao, Ph.D. My laboratory investigates the molecular mechanisms regulating neurodevelopment. Using mouse genetics and human pluripotent stem cells as models, we interrogate the mechanism underlying impaired neurogenesis in neurodevelopmental disorders. One of the proteins that we are studying is Fragile X mental retardation protein (FMRP), a brain-enriched RNA-binding protein. Functional loss of FMRP leads to Fragile X syndrome, the most common monogenetic form of inherited intellectual disability and the largest single genetic contributor to autism. We have discovered that FMRP regulates postnatal and adult neurogenesis and uncovered underlying mechanisms such as altered epigenetic state and mitochondrial dysfunction. Our work has unveiled a number of novel therapeutic targets for neurodevelopmental disorders.

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Sep

30

Allosteric Modulation of Glutamate Receptors

Chicago - 4:00 PM - 5:00 PM

Stephen F Traynelis, Ph.D.Professor of Pharmacology and Chemical BiologyEmory University School of Medicine Abstract:NMDA receptors mediate a slow, Ca2+-permeable component of excitatory synaptic transmission in the central nervous system (CNS). These receptors are ligand-gated ion channels that are tetrameric assemblies of two glycine-binding GluN1 subunits and two glutamate-binding GluN2 subunits. There are four different genes encoding GluN2 (GRIN2A, GRIN2B, GRIN2C, GRIN2D), which are each expressed with a unique spatial profile throughout the CNS at different developmental stages. The different GluN2 subunits control the temporal signaling properties of the receptors, which likely allows different subunits to mediate different roles in development and circuit function. NMDA receptors require the binding of both glutamate and glycine in order to open the pore, which is triggered by protein rearrangements secondary to agonist-induced closure of a bi-lobed agonist binding domain that resembles a clamshell. We hypothesize that three key gating elements control opening of the ion-conducting pore following agonist binding. These elements include the 9 highly conserved residues (SYTANLAAF) that comprise the extracellular end of the M3 transmembrane helix, the short two turn helix that is parallel to the plane of the membrane and precedes the M1 transmembrane helix, and the short linker preceding the M4 transmembrane helix (Amin et al., 2018; Chen et al., 2017; Gibb et al., 2018, Yuan et al., 2014). A considerable amount of data implicates these regions in gating, including the observation that regions of the genes encoding these portions of the polypeptide chain are devoid of variation in the human population, yet are a locus for disease-causing mutations in patients with neurological disease (XiangWei et al., 2018). We have studied the functional consequences of these de novo mutations, which have diverse effects on the process of channel gating. Our results included the identification of a mutation in the pre-M1 helix that reduced single channel conductance (Ogden et al., 2017), which is rare for receptor mutations that lie outside of the pore-forming regions. These data suggest that the pre-M1 helix may influence the geometry and characteristics of the open pore. Consistent with this idea, we have identified several allosteric modulators that appear to act at the pre-M1 region and can also reduce single channel conductance, an effect not previously observed for exogenous modulators of NMDA receptor function. For example, the thienopyrimidone EU1622 series of positive allosteric modulators of NMDA receptor function (Perszyk et al., Soc Neuroscience Annual Meeting, 2014) have structural determinants in the pre-M1 region. Members of this class can reduce single channel conductance while still potentiating the maximally effective current. Chord conductance levels of NMDA receptors on cultured cortical neurons changed from 52, 44 pS in vehicle (0.2% DMSO) to 42, 35, and 28 pS in 50 M EU1622-14 (mean from 7 outside out patches recorded at -80 mV, SEM varied between 0.5-1.1 pS). Given that the pre-M1 region might influence the properties of the pore, we explored the mechanism underlying this effect, and discovered that one modulator that reduces conductance can also alter the relative permeability ratio for cations. We found that EU1622-14 reduced the relative permeability of Ca2+ to Na+ for recombinant GluN1/GluN2A and GluN1/GluN2B receptors expressed in HEK cells by more than 2-fold (p<0.05 for both receptors, One-way ANOVA, post-hoc t-test of drug vs vehicle, Bonferroni correction for multiple comparisons, F3,28 = 6.91). This represents the first example to our knowledge of an exogenous drug-like allosteric modulator that can interact with the NMDAR protein complex to alter the relative permeability of ions, which has important implications. The result is perhaps intuitively understandable, as any change in the diameter or electrostatic properties of the pore that alters unitary conductance would be unlikely to do so in a manner that equally affects the permeability of ions with different diameters and distinct hydration shells. Rather, it seems likely that ions with unique atomic radii will have a different relative permeability when the pore diameter or electrostatic environment changes. These findings highlight important biophysical considerations about how the NMDA receptor tetrameric complex controls pore diameter and related properties. In addition, the precedent that Ca2+ permeability can be controlled pharmacologically creates a new potential therapeutic target (i.e. regulation of ionic selectivity) with intriguing possibilities, such as future development of positive allosteric modulators of NMDA receptor function that do not elevate intracellular Ca2+ to potentially pathological levels.  

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Oct

03

BMG Seminar: Chaperone discovery and characterization -James Bardwell, PhD

Chicago - 10:00 AM - 11:00 AM

Protein folding in the cell relies heavily on chaperones. Even though much has been learned about chaperones, particularly in regard to their co-chaperone and co-factor requirements, observing how chaperones bind to a wide range of substrate proteins and affect their folding has proven to be very difficult. This difficulty primarily comes from two sources: the functional complexity of chaperone machines, and the fact that chaperone substrates are almost always poorly defined mixtures of partially structured folding intermediates. We decided to embark on a chaperone discovery journey with the aim of finding chaperones that are simpler and more biophysically tractable than those currently studied. Ideally, these new chaperones should act on a substrate protein whose folding mechanism is already well characterized, so that we candetermine precisely how the chaperone is affecting the folding of the substrate. We thus developed genetic selections that directly link the stability of model folding proteins to increased antibiotic resistance in vivo. The folding biosensors that we have developed function in the bacterial periplasm and cytosol, and in yeast. These biosensors have allowed us to optimize protein folding and discover new chaperones we used the first of our discovered chaperones, Spy, as a model to delve deeply into chaperone biology and we now understand, in unprecedented detail, how this chaperone interacts with client proteins to facilitate their folding. We are following our chaperone discovery efforts into yeast with the aim of addressing the role that host factors play in amyloid formation, which is linked to a number of devastatingneurological diseases. James C. Bardwell, PhDRowena G. Matthews Collegiate Professor, Department of Molecular, Cellular, and Developmental BiologyProfessor, Department of Biological ChemistryUniversity of Michigan Howard Hughes Medical Institute Investigator  

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Oct

03

Disruption of Synaptic Transmission and Plasticity in Cognitive Disorders - Richard L. Huganir, PhD

Chicago - 2:00 PM - 3:00 PM

The Center for Autism and Neurodevelopment of Northwestern University Feinberg School of Medicine welcomes you to attend a lecture featuring: Richard L. Huganir, PhDBloomberg Distinguished Professor of Neuroscience and Psychological and Brain SciencesDirector, Solomon H. Snyder Department of NeuroscienceCo-Director, Brain Science InstituteJohns Hopkins University School of MedicineNeurotransmitter receptors mediate signal transduction at synaptic connections between neurons in the brain and the regulation of receptor function is critical for synaptic plasticity. My laboratory has been elucidating the molecular mechanisms underlying the regulation of AMPA receptors, the major excitatory neurotransmitters receptors in the central nervous system. We have found that AMPA receptors are extensively posttranslationally modified by phosphorylation, palmitoylation and ubiquination. Protein phosphorylation is a major form of AMPA receptor regulation and the receptors are phosphorylated on serine, threonine and tyrosine residues by many different protein kinases. We have shown that phosphorylation of the receptor regulates its ion channel properties and membrane trafficking and that receptor phosphorylation is critical for the expression of several forms of synaptic plasticity and for learning and memory. We have also identified a variety of AMPA receptor interacting proteins, including GRIP1/2, PICK1, GRASP1, SNX27, KIBRA, and SynGAP1 that interact with AMPA receptors and are necessary for their proper subcellular trafficking. This AMPA receptor complex is important for several forms of synaptic plasticity and learning and memory. These studies indicate that the modulation of receptor function is a major mechanism for the regulation of synaptic transmission and is a critical determinant of animal behavior. Recent evidence has indicated that AMPA receptor function may be disrupted in several neuropsychiatric disorders. Specifically, mutations in SynGAP, GRIP1 and GRASP1 as well as AMPA receptor subunits have been found to be associated with cognitive disorders including intellectual disability, autism, and schizophrenia. SynGAP1 loss of function mutations are now thought to underlie 1% of intellectual disabilities. Recently we have characterized these disease-associated SynGAP1 mutations to examine their effect on SynGAP protein function, AMPA receptor trafficking, synaptic plasticity and behavior and are developing potential therapeutic approaches to treat these devastating disorders. Dr. Richard Huganir is a Bloomberg Distinguished Professor of Neuroscience and Psychological and Brain Sciences and Director of the Solomon H. Snyder Department of Neuroscience at the Johns Hopkins School of Medicine where he is also the Co-Director of the Johns Hopkins Medicine Brain Science Institute. Dr. Huganir received his Ph.D. degree in Biochemistry, Molecular and Cell Biology from Cornell University in 1982 where he performed his thesis research in the laboratory of Dr. Efraim Racker. He was a postdoctoral fellow with the Nobel Laureate, Dr. Paul Greengard, at Yale University School of Medicine from 1982-1984. Dr. Huganir then moved to the Rockefeller University where he was an Assistant Professor of Molecular and Cellular Neurobiology from 1984-1988. Dr. Huganir moved to the Johns Hopkins University School of Medicine in 1988 as an Associate Investigator in the Howard Hughes Medical Institute and an Associate Professor in the Department of Neuroscience. Dr. Huganir was an Investigator with the Howard Hughes Medical Institute from 1988-2014. Dr. Huganir became the Director or the Solomon H. Snyder Department of Neuroscience in 2006. Dr. Huganir’s career has focused on synapses, the connections between nerve cells, in the brain. Dr. Huganir’s studies have shown that the regulation of receptor function is a major mechanism for the regulation of neuronal excitability and connectivity in the brain and is critical for many higher brain processes, including learning and memory, and is a major determinant of behavior. Moreover, dysregulation of these mechanisms underlie many neurological and psychiatric diseases including Alzheimer’s, ALS, schizophrenia, autism, intellectual disability, PTSD as well as in chronic pain and drug addiction. Dr. Huganir is currently the Chair of the Stanley Center for Psychiatric Research Scientific Advisory Committee and a recent member of the NIMH Council and on the NIH BRAIN Multi-Council Working Group. Dr. Huganir is a past President of the Society for Neuroscience and has served as Treasurer of the Society for Neuroscience. He has received the Young Investigator Award and the Julius Axelrod Award from the Society for Neuroscience, the Santiago Grisolia Award, the Goldman-Rakic Award, the Edward M. Scolnick Prize in Neuroscience and is a fellow of the American Association for the Advancement of Science, a member of the American Academy of Arts and Sciences, the National Institute of Medicine and the National Academy of Sciences.

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Oct

10

BMG Seminar: Immortal Hematopoietic Stem Cells and Their Regulation by DNA Methylation - Peggy Goodell, PhD

Chicago - 10:00 AM - 11:00 AM

The peripheral blood is composed of many different cell types which are constantly being replenished via hematopoietic stem cells (HSCs). When young, thousands of hematopoietic stem cells residing in the bone marrow are simultaneously regenerating the blood. Over the past few years, high throughput sequencing has revealed that as we age, one or a few stem cells start dominating blood production, resulting in a condition termed “clonal hematopoiesis”, or “CH”. CH represents blood production from “immortal” stem cells that outcompete their normal counterparts. CH is driven by somatically acquired mutations in around 20 genes which confer a selective advantage over time. The gene encoding DNA methyltransferase 3A (DNMT3A) is the most commonly mutated gene in CH, indicating that loss of its function confers longevity on the stem cell, even as it puts the host at risk for age-associated diseases such as leukemia. Dr. Goodell will discuss some of the cellular and molecular mechanisms that drive expansion of HSCs with DNMT3A and other CH-associated mutations. Peggy Goodell, PhDProfessor, Department of PediatricsProfessor, Department of Molecular and Human GeneticsVivian L. Smith Chair in Regenerative MedicineBaylor College of Medicine  

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Oct

10

Neena B. Schwartz Memorial Lectureship featuring Dr. Dan Bernard

Chicago - 4:00 PM - 5:30 PM

For the past 15 years, the Center for Reproductive Science has celebrated the life and work of our founder, Professor Neena B. Schwarz, with our annual NBS Lecture in Reproductive Science. On October 10th, 2019, we welcome Dr. Dan Bernard, Professor, Department of Pharmacology & Therapeutics, and Director, McGill Centre for Research in Reproduction and Development, McGill University, Montreal Canada. On April 15th, 2018, Professor Neena B. Schwartz, The William Deering Professor of Endocrinology Emerita at Northwestern University, passed away peacefully at the age of 91. We will continue to celebrate her legacy through the Neena B. Schwartz Memorial Lectureship, which will be held in in Fall 2018, more information on this lecture to follow. Dontations continue to be accepted for this lectureship.

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Oct

11

Stem Cells & Regenerative Biology Seminar Series

Chicago - 12:00 PM - 1:00 PM

Presented By: Celeste Nelson, PhDDepartment of Chemical & Biological EngineeringPrinceton University, NJ  

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Oct

14

Identification and Therapeutic Targeting of Breast Cancer Metastasis Genes

Chicago - 4:00 PM - 5:00 PM

Yibin Kang, Ph.D.Warner-Lambert/Parke-Davis Professor of Molecular BiologyPrinceton University Abstract:Breast cancer remains a significant health concern worldwide. Our previous studies suggested that Metadherin (MTDH) promotes breast cancer initiation, progression, and treatment resistances. However, whether targeting MTDH has therapeutic potential is still elusive. Using inducible Mtdh knockout mouse models we found that MTDH sustains breast cancer progression and metastasis via interacting with SND1, and acute Mtdh loss inhibits breast cancer development. Through high throughput screenings, we obtained a serial of MTDH/SND1 inhibitors. Treatments of the compounds suppress breast tumor growth, metastasis, and sensitize breast cancer to chemotherapy by sensitize cancer cells to stress-induced apoptosis.  Our results suggest that targeting MTDH/SND1 complex could have therapeutic potential and compounds that disrupt the interaction may be developed as novel therapeutic agents for breast cancer.

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Oct

15

Center for Translational Pain Research Launch

Chicago - 11:00 AM - 12:30 PM

Please join us for the launch of the Center for Translational Pain Research at Northwestern University Feinberg School of Medicine! KEYNOTE SPEAKER:Jon-Kar Zubieta, MD, PhDProfessor of PsychiatryStony Brook University  FEATURING:A. Vania Apkarian, PhDDirector, Center for Translational Pain ResearchProfessor of Physiology, Anesthesiology, and Physical Medicine and RehabilitationNorthwestern University Feinberg School of Medicine Rex Chisholm, PhDVice Dean for Scientific Affairs and Graduate EducationAdam and Richard T. Lind Professor of Medical GeneticsProfessor of Cell and Developmental Biology and SurgeryNorthwestern University Feinberg School of Medicine  Yu Lin, MD, PhDProgram Director, Cognitive Neuroscience, NeuroAIDS, Human PainNational Institute on Drug Abuse (NIDA)Division of Neuroscience and Behavior, Integrative Neuroscience Branch

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Oct

17

BMG Seminar: Metabolic control of cell growth through the PI3K-mTOR signaling network - Brendan Manning, PhD

Chicago - 10:00 AM - 11:00 AM

The mechanistic target of rapamycin (mTOR) complex 1 (mTORC1) is a key signaling node, universal to eukaryotic cells, which links the sensing of nutrients to the coordinated regulation of nutrient metabolism. mTORC1 has the ability to integrate signals from a variety of sources, including intracellular nutrients and secreted growth factors. The activation state of mTORC1 is tightly controlled through a small G protein switch involving the TSC1-TSC2-TBC1D7 complex (the TSC complex) and the Ras-related small G protein Rheb. The direct phosphorylation and inhibition of the TSC complex by the protein kinase Akt provides the major mechanistic link between growth factor signaling and mTORC1. Current evidence indicates that this signal is integrated with amino acid sensing pathways upstream of mTORC1 through independent spatial control over the subcellular localization of the TSC complex and mTORC1 to the surface of the lysosome. Our data indicate that both physiological growth signals and common oncogenic events in cancer activate mTORC1 through mechanisms leading to dissociation of the TSC protein complex from the lysosomal subpopulation of Rheb, which is required for mTORC1 activation. Physiological and pathological activation of PI3K-mTOR signaling results in a shift from catabolic processes to anabolic biosynthetic processes. This pathway acutely responds to feeding and is also frequently and aberrantly activated in human cancers. Through unbiased genomic and metabolomic approaches, we have found that, in addition to its established roles in promoting protein synthesis and inhibiting autophagy, mTORC1 stimulates changes in specific metabolic pathways through transcriptional and posttranslational effects on metabolic enzymes. In this manner, mTORC1 serves to link growth signals to metabolic processes that promote the growth of cells, tissues, and tumors, including the de novo synthesis of proteins, lipids, and nucleotides. Research in our lab is focused on understanding the coordinated anabolic program downstream of PI3K-mTOR signaling and identifying metabolic vulnerabilities stemming from uncontrolled pathway activation that can be targeted in tumors. I will discuss our latest data on additional metabolic enzymes under control of the PI3K-mTOR network that contribute to an integrated metabolic program underlying cell growth in both normal and cancer cells. Brendan Manning, PhDProfessor, Department of Genetics and Complex DiseasesDirector of the Division of Biological SciencesDirector of the PhD Program in Biological Sciences in Public Health, Harvard Graduate School of Arts and SciencesHarvard T.H. Chan School of Public Health  

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Oct

18

NU GoKidney Innovation Symposium: The Revolution in Kidney Medicine

Chicago - 8:30 AM - 5:00 PM

Join Northwestern's George M. O'Brien Kidney Research Core Center (NUGoKidney) for it's first Innovation Symposium.  Featuring the leading experts reshaping the future of kidney research, this full day of presentations and discussions will explore the latest innovative technologies and therapeutics in kidney disease and examine how these new breakthroughs could translate to a future beyond kidney disease. More exciting details to come! Keep an eye on our website and follow us on Twitter @NU_Nephrology to get the latest information. We hope you will join us for this exciting, interactive event!

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Oct

21

CatSper: The Ca2+ Channel in the Sperm Function

Chicago - 4:00 PM - 5:00 PM

Jean Ju Chung, Ph.D.Assistant Professor of Cellular & Molecular PhysiologyYale School of Medicine Abstract:To achieve fertilization, sperm must have properly functioning Ca2+ signaling. Ca2+ influx into the flagellum is required for sperm to hyperactivate, an asymmetric flagellar movement necessary for mammalian sperm navigation and egg penetration. Varying pH of luminal fluid along the female reproductive tract is a physiological cue that modulates the sperm motility. CatSper is a sperm-specific, pH-sensitive calcium channel essential for hyperactivated motility and male fertility. Multi-subunit CatSper channel complexes organize linear Ca2+ signaling nanodomains along the sperm tail. Here we report a pH-dependent calcium sensor that enables modulation of CatSper channel and the sperm motility in response to changing conditions along the female reproductive tract.

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Oct

24

BMG Seminar: Maintaining Genome Stability During DNA Replication -David Cortez, PhD

Chicago - 10:00 AM - 11:00 AM

Billions of base pairs of DNA must be replicated trillions of times during a human lifetime. Adding to the difficulty, thousands of DNA lesions happen in each cell of our body every day. Furthermore, replication is challenged by difficult to replicate sequences and conflicts with transcription. To combat these threats, DNA damage response mechanisms act to repair the damaged DNA, signal cell cycle checkpoint activation, ensure completion of DNA replication, and maintain genome stability. Defects in these mechanisms cause developmental abnormalities, premature aging, and cancer. We have utilized a proteomic approach invented by a former graduate student called iPOND to inventory and track ~600 proteins that act at active and damaged replication forks. This approach identified proteins including ETAA1, RADX, and HMCES that act in different replication-stress response pathways. I will present our latest discoveries about how these proteins function to maintain genome stability. David Cortez, PhDProfessor, Department of BiochemistryIngram Professor of Cancer ResearchCo-Leader, Genome Maintenance Program, Vanderbilt-Ingram Cancer CenterVanderbilt University School of Medicine  

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Oct

25

BMG Journal Club

Chicago - 3:30 PM - 5:00 PM

The BMG Journal Club will convene every other Friday from 3:30pm to 5:00pm. This is an opportunity for the department to come together and have in-depth discussions about the current literature and the overall implications of new studies, enhancing everyone’s knowledge of the field at large and about each other’s research interests within the department; providing possible opportunities to collaborate as well. This is also an opportunity to practice vital presentation skills in front of a friendly audience. Pizza and soda will be served.

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Oct

31

BMG Seminar: Setting Boundaries: How cells keep telomeres in check -Eros Lazzerini Denchi, PhD

Chicago - 10:00 AM - 11:00 AM

The Department of Biochemistry and Molecular Genetics Departmental Seminar Series presents: Eros Lazzerini Denchi, PhDInvestigator, Laboratory of Genome IntegrityNIH Stadtman InvestigatorCenter for Cancer Research, National Cancer InstituteNational Institutes of Health  

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Nov

07

BMG Seminar: Computation, Memory, and Complexity: Design of Gene Regulatory Circuits in Eukaryotic Cells - Ahmad (Mo) Khalil, PhD

Chicago - 10:00 AM - 11:00 AM

Eukaryotic organisms display diverse genetic responses to the environment. These complex responses are mediated by genetic regulatory circuits that enable cells to perform core functions, such as process signals, execute computations, and store memory. What molecular circuit designs enable these core functions, and how do regulatory circuits evolve? How do we engineer synthetic circuits to program desired cellular functionality? To address these questions, my lab primarily employs synthetic biology approaches and develops new laboratory technologies. This talk will explore eukaryotic transcriptional circuit design principles from a synthetic biology perspective. I will describe a new approach for engineering fully artificial transcriptional and epigenetic circuits that explore and exploit common natural regulatory features, such as cooperative transcription factor (TF) assembly and reading / writing chromatin modifications. In addition, I will present a highly flexible and automated, continuous culture platform we invented, called eVOLVER, that allows researchers to grow and experimentally evolve natural and synthetic cellular systems in highly defined growth conditions. Ahmad (Mo) Khalil, PhDAssistant Professor, Department of Biomedical EngineeringAssociate Director, Biological Design CenterRajen Kilachand Center for Integrated Life Sciences & EngineeringBoston University  

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Nov

08

Stem Cells & Regenerative Biology Seminar Series

Chicago - 12:00 PM - 1:00 PM

Presented By: Mark Krasnow, MD, PhDHHMI InvestigatorDepartment of Biochemistry, Stanford University School ofMedicine California  

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Nov

08

Pain, Action and Interference - Johan W.S. Vlaeyen, PhD

Chicago - 12:30 PM - 1:30 PM

Johan W.S. Vlaeyen, PhDProfessor of Health Psychology, KU Leuven University, BelgiumProfessor of Experimental Health Psychology, Maastricht University, NetherlandsAdjunct Research Professor, University of South Australia, Adelaide 

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Nov

08

BMG Journal Club

Chicago - 3:30 PM - 5:00 PM

The BMG Journal Club will convene every other Friday from 3:30pm to 5:00pm. This is an opportunity for the department to come together and have in-depth discussions about the current literature and the overall implications of new studies, enhancing everyone’s knowledge of the field at large and about each other’s research interests within the department; providing possible opportunities to collaborate as well. This is also an opportunity to practice vital presentation skills in front of a friendly audience. Pizza and soda will be served.

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Nov

11

BMG Distinguished Lecturer: Geeta Narlikar, PhD

Chicago - 10:00 AM - 11:00 AM

The Department of Biochemistry and Molecular Genetics presents: Geeta Narlikar, PhDProfessor of Biochemistry and BiophysicsLewis and Ruth Cozen ChairUniversity of California, San Francisco

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Nov

11

Pharmacology Seminar: Baron Chanda, Ph.D.

Chicago - 4:00 PM - 5:00 PM

Baron Chanda, Ph.D.Professor of NeuroscienceUniversity of Wisconsin-Madison

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Nov

14

CANCELLED - BMG Seminar: Sara Buhrlage, PhDBMG Seminar: Sara Buhrlage, PhD

Chicago - 10:00 AM - 11:00 AM

The Department of Biochemistry and Molecular Genetics Departmental Seminar Series presents: Sara Buhrlage, PhDAssistant Professor, Biological Chemistry and Molecular PharmacologyHarvard Medical SchoolAssistant Professor, Cancer BiologyDana-Farber Cancer Institute  

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Nov

14

CANCELLED - CANCELED: Center for Autism and Neurodevelopment seminar - Roger Nicoll, MDCANCELED: Center for Autism and Neurodevelopment seminar - Roger Nicoll, MD

Chicago - 2:00 PM - 3:00 PM

The Center for Autism and Neurodevelopment of Northwestern University Feinberg School of Medicine welcomes you to attend a lecture featuring: Roger Nicoll, MDProfessor of Cellular Molecular PharmacologyUniversity of California, San Francisco

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Nov

18

Pharmacology Seminar: Indira M. Raman, Ph.D.

Chicago - 4:00 PM - 5:00 PM

Indira M. Raman, Ph.D.Bill and Gayle Cook Professor of NeurobiologyNorthwestern University

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Nov

21

BMG Seminar: The Signaling and Metabolic Landscape Associated with Metastatic Progression - John Blenis, PhD

Chicago - 10:00 AM - 11:00 AM

It is known that primary solid tumors are generally not the cause of cancer-related deaths but that 80-90% of mortality is the result of cancer cells gaining the ability to leave the primary tumor, activate survival processes, invade surrounding tissues, intravasate into the circulation, extravasate into new tissues, and form secondary tumors, often after long latencies. We have discovered that distinct ERK substrate recognition domains make major contributions to specific cancer phenotypes such as proliferation versus metastatic progression. While much is known regarding ERK proliferative signaling mechanisms, much less is understood regarding the role of ERK signaling in the acquisition of metastatic properties. Therefore, defining the signaling mechanisms and biological outcomes downstream of ERK that contribute to the development of metastasis are of critical importance. To discover new processes linked to the initiation and establishment of the metastatic phenotype, we have completed several large-scale screening efforts (gene expression arrays, proteomics, phosphoproteomics, and metabolomics) aimed at mapping the temporal changes that occur during ERK2-driven acquisition of aggressive, mesenchymal phenotypes. These approaches have yielded several new discoveries such as mechanisms of cross-talk between ERK2 and TGFb pathways, chromatin remodeling through regulation of histone chaperones, metabolic reprogramming and identification of metabolites acting as second messengers that drive aging-associated metastasis. How ERK2 and TGFb contribute to chromatin remodeling and metabolic reprogramming will be discussed. John Blenis, PhDAnna Maria and Stephen Kellen Professor of Cancer ResearchProfessor, Department of PharmacologyAssociate Director of Basic Science, Sandra and Edward Meyer Cancer CenterWeill Cornell Medicine  

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Nov

22

BMG Journal Club

Chicago - 3:30 PM - 5:00 PM

The BMG Journal Club will convene every other Friday from 3:30pm to 5:00pm. This is an opportunity for the department to come together and have in-depth discussions about the current literature and the overall implications of new studies, enhancing everyone’s knowledge of the field at large and about each other’s research interests within the department; providing possible opportunities to collaborate as well. This is also an opportunity to practice vital presentation skills in front of a friendly audience. Pizza and soda will be served.

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Nov

25

SQE Distinguished Lecturer: Yi Zhang, PhD

Chicago - 10:00 AM - 11:00 AM

The Simpson Querrey Center for Epigenetics presents: Yi Zhang, PhDFred Rosen Professor, Department of Genetics & Pediatrics, HMS & BCH Investigator, Howard Hughes Medical Institute  

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Nov

25

Serotonergic Monitoring of Peripheral Inflammation: Clues to an Autism Treatment?

Chicago - 4:00 PM - 5:00 PM

Randy D. Blakely, Ph.D.Executive Director of FAU Brain InstituteProfessor of Biomedical ScienceFlorida Atlantic University Epidemiological, post-mortem and gene network analyses have pointed to changes in inflammatory signaling pathways as a contribution to risk of autism. How such changes lead to alterations in brain development and function remain ill-defined. Previously, we identified an IL-1R activated p38α MAPK signaling pathway as central to the posttranslational control of serotonin signaling via modulation of presynaptic serotonin transporter (SERT) function, consistent with recent findings of significant expression of Il-1Rs by serotonin neurons. The possibility that an IL-1R/p38α MAPK/SERT signaling pathway might have disease relevance became of interest with our identification in subjects with autism of multiple, rare, hyperfunctional SERT coding variants that display constitutive p38α MAPK-dependent activation. With a knock-in mouse expressing the most common of these variants, SERT Ala56, we demonstrated elevated CNS serotonin clearance in vivo, and demonstrate changes in CNS and GI physiology and behavior consistent with constitutive-activation of SERT function. Recently, using brain penetrant, isoform-specific, p38α MAPK inhibitors, as well as conditional, serotonin neuron-specific elimination of p38α MAPK, we have been able to normalize multiple changes in these mice. Together, our studies point to the normal use of an IL-1R/p38α MAPK signaling pathway targeting SERT in serotonin neurons to modulate behavior in response to CNS and/or peripheral innate immune system activation. Inappropriate or excessive activation of this pathway during early life may contribute to one or more facets of autism that may be manipulated through pharmacological p38α MAPK inhibition.

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Dec

02

Pharmacology Seminar: Geoffrey W. Abbott, Ph.D.

Chicago - 4:00 PM - 5:00 PM

Geoffrey W. Abbott, Ph.D.Professor of Pharmacology, Physiology and BiophysicsUniversity of California – Irvine

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Dec

05

BMG Seminar: Nrf2 activation promotes lung cancer metastasis by inhibiting the Fbxo22-mediated degradation of Bach1 -Michele Pagano, MD

Chicago - 10:00 AM - 11:00 AM

About 30% of lung adenocarcinomas (LUADs) increase the transcription of antioxidant genes to maintain oxidative homeostasis. This increase is made possible by mutations that stabilize Nrf2, the master transcriptional regulator of the cell’s antioxidant program. These mutations are associated with an aggressive cancer phenotype and either directly target Nfe2L2 (encoding Nrf2) or inactivate Nrf2’s negative regulator, Keap1. Keap1 is a substrate receptor of a CRL3 ubiquitin ligase complex that, in physiological conditions, constitutively targets Nrf2 for degradation. We asked whether LUADs with Keap1 mutations are more aggressive than LUADs harboring wild-type Keap1 due to an increased metastatic burden, and by which mechanism. We found that stabilization of Nrf2 in LUAD activates a pathway that in turn stabilizes Bach1, a transcription factor that controls the expression of a plethora of pro-metastatic genes. Mechanistically, mutations that stabilize Nrf2 drive the Nrf2-mediated induction of heme oxygenase 1 (Ho1), an enzyme responsible for heme catabolism. We also found that heme promotes the interaction of Bach1 with CRL1Fbxo22. Therefore, increased heme catabolism leads to a decrease in free heme, reducing the CRL1Fbxo22-mediated degradation of Bach1. Thus, in normal cells, either Nrf2 is low and Bach1 is high (under unstressed conditions) or Nrf2 is high and Bach1 is low (upon oxidative stress). Instead, LUAD cells paradoxically display high levels of both Nrf2 and Bach1, thus promoting cell survival and inducing cell migration, respectively. We extensively validated our mechanistic results in mouse models of LUAD, as well as in samples of LUAD patients. We propose that: 1) Nrf2 induces lung cancer metastases by reducing heme- and Fbxo22-mediated degradation of Bach1, which in turn activates the transcription of pro-metastatic genes; and 2) drugs targeting the heme pathway represent a promising strategy to block metastasis in LUAD patients. Moreover, we suggest that Ho1 and Bach1 could be used as LUAD biomarkers to improve the design of precision medicine approaches and clinical trials, and to monitor the response to therapy. Michele Pagano, MDChair, Department of Biochemistry and Molecular PharmacologyMay Ellen and Gerald Jay Ritter Professor of Oncology, Department of Biochemistry and Molecular PharmacologyNew York University School of MedicineHoward Hughes Medical Institute Investigator  

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Dec

06

BMG Distinguished Lecturer: Karen Vousden, PhD

Chicago - 10:00 AM - 11:00 AM

The Department of Biochemistry and Molecular Genetics presents: Karen Vousden, PhDChief Scientist, CRUK Group Leader, Francis Crick Institute, London

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Dec

06

Center for Translational Pain Research Seminar - Giandomenico Iannetti, MD, PhD

Chicago - 12:00 PM - 1:00 PM

Giandomenico Iannetti, MD, PhDProfessor of NeuroscienceNeuroscience and Behaviour LaboratoryIstituto Italiano di Tecnologia (IIT), RomeDepartment of Neuroscience, Physiology & PharmacologyUniversity College London 

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Dec

09

SQE Distinguished Lecturer: Luciano Di Croce, PhD

Chicago - 10:00 AM - 11:00 AM

The Simpson Querrey Center for Epigenetics presents: Luciano Di Croce, PhDICREA Research Professor at Centre de Regulació Genòmica (CRG)Life & Medical Sciences, Barcelona  

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Dec

19

Center for Translational Pain Research Seminar - Jose Moron-Concepcion, PhD

Chicago - 10:30 AM - 11:30 AM

Jose Moron-Concepcion, PhDProfessor of Anesthesiology, Neuroscience & PsychiatryWashington University Pain CenterWashington University School of Medicine

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