Vanderbilt Center for Stem Cell Biology

Mission Statement

The Vanderbilt Center for Stem Cell Biology (VCSCB) is a participation-based entity that brings together investigators interested in stem and/or progenitor cell biology. By stimulating scientific interactions, we strive to broadly propel and elevate the generation of new knowledge related to tissue and organ development with strong emphasis on the cellular and genetic mechanisms that regulate cell fate specification, plasticity and maintenance.

Goals and Activities

Our goal is to advance individual and team-based research activities that relate to stem and progenitor-cell biology. To do so, we place a high priority on graduate and post-doctoral training, the exchange of state-of-the-art knowledge, and the oversight of two shared resources that provide access to critical technology. To enhance graduate and post-doctoral training, we co-operate with the trans-institutional Vanderbilt Program in Developmental Biology, led by Dr. Chris Wright. To exchange state-of-the-art knowledge, we organize and host the bi-weekly SPRING seminar series, and periodically bring in external speakers, either in co-operation with the departmental Cell & Developmental Biology seminar series, or by organizing day-long VCSCB Symposia with internationally renowned speakers. To provide easy access to key technological tools and strategies, both the Vanderbilt Genome-Editing Resource (VGER) and Creative Data Solutions (CDS) reside within this Center.

Core Principle

We are dedicated to training the next generation of scientists. This requires that we place a high priority on discovery science, creative scholarship, effective communication, and high-impact publication.

Featured Collections

• Information

Publications

Featured publications

1. Glucose Regulates Microtubule Disassembly and the Dose of Insulin Secretion via Tau Phosphorylation. Ho KH, Yang X, Osipovich AB, Cabrera O, Hayashi ML, Magnuson MA, Gu G, Kaverina I (2020) Diabetes 69(9): 1936-1947
   › Primary publication · 32540877 (PubMed) · PMC7458041 (PubMed Central)
2. Myt Transcription Factors Prevent Stress-Response Gene Overactivation to Enable Postnatal Pancreatic β Cell Proliferation, Function, and Survival. Hu R, Walker E, Huang C, Xu Y, Weng C, Erickson GE, Coldren A, Yang X, Brissova M, Kaverina I, Balamurugan AN, Wright CVE, Li Y, Stein R, Gu G (2020) Dev Cell 53(4): 390-405.e10
   › Primary publication · 32359405 (PubMed) · PMC7278035 (PubMed Central)
3. Excitotoxicity and Overnutrition Additively Impair Metabolic Function and Identity of Pancreatic β-Cells. Osipovich AB, Stancill JS, Cartailler JP, Dudek KD, Magnuson MA (2020) Diabetes 69(7): 1476-1491
   › Primary publication · 32332159 (PubMed) · PMC7809715 (PubMed Central)
4. Coregulator Sin3a Promotes Postnatal Murine β-Cell Fitness by Regulating Genes in Ca Homeostasis, Cell Survival, Vesicle Biosynthesis, Glucose Metabolism, and Stress Response. Yang X, Graff SM, Heiser CN, Ho KH, Chen B, Simmons AJ, Southard-Smith AN, David G, Jacobson DA, Kaverina I, Wright CVE, Lau KS, Gu G (2020) Diabetes 69(6): 1219-1231
   › Primary publication · 32245798 (PubMed) · PMC7243292 (PubMed Central)
5. Gene network transitions in embryos depend upon interactions between a pioneer transcription factor and core histones. Iwafuchi M, Cuesta I, Donahue G, Takenaka N, Osipovich AB, Magnuson MA, Roder H, Seeholzer SH, Santisteban P, Zaret KS (2020) Nat Genet 52(4): 418-427
   › Primary publication · 32203463 (PubMed)
6. Retraction Note: Transient cytokine treatment induces acinar cell reprogramming and regenerates functional beta cell mass in diabetic mice. Baeyens L, Lemper M, Leuckx G, De Groef S, Bonfanti P, Stangé G, Shemer R, Nord C, Scheel DW, Pan FC, Ahlgren U, Gu G, Stoffers DA, Dor Y, Ferrer J, Gradwohl G, Wright CVE, Van de Casteele M, German MS, Bouwens L, Heimberg H (2020) Nat Biotechnol 38(3): 374
   › Primary publication · 32066957 (PubMed) · PMC7175803 (PubMed Central)
7. Inactivation of mTORC2 in macrophages is a signature of colorectal cancer that promotes tumorigenesis. Katholnig K, Schütz B, Fritsch SD, Schörghofer D, Linke M, Sukhbaatar N, Matschinger JM, Unterleuthner D, Hirtl M, Lang M, Herac M, Spittler A, Bergthaler A, Schabbauer G, Bergmann M, Dolznig H, Hengstschläger M, Magnuson MA, Mikula M, Weichhart T (2019) JCI Insight 4(20)
   › Primary publication · 31619583 (PubMed) · PMC6824305 (PubMed Central)
8. Prevention and Reversion of Pancreatic Tumorigenesis through a Differentiation-Based Mechanism. Krah NM, Narayanan SM, Yugawa DE, Straley JA, Wright CVE, MacDonald RJ, Murtaugh LC (2019) Dev Cell 50(6): 744-754.e4
   › Primary publication · 31422917 (PubMed) · PMC6776997 (PubMed Central)
9. Differential Cell Susceptibilities to Kras in the Setting of Obstructive Chronic Pancreatitis. Shi C, Pan FC, Kim JN, Washington MK, Padmanabhan C, Meyer CT, Kopp JL, Sander M, Gannon M, Beauchamp RD, Wright CV, Means AL (2019) Cell Mol Gastroenterol Hepatol 8(4): 579-594
   › Primary publication · 31310834 (PubMed) · PMC6889613 (PubMed Central)
10. Regulation of Glucose-Dependent Golgi-Derived Microtubules by cAMP/EPAC2 Promotes Secretory Vesicle Biogenesis in Pancreatic β Cells. Trogden KP, Zhu X, Lee JS, Wright CVE, Gu G, Kaverina I (2019) Curr Biol 29(14): 2339-2350.e5
    › Primary publication · 31303487 (PubMed) · PMC6698911 (PubMed Central)

Community Leaders

• Mark Magnuson
  Director
• Jean-Philippe Cartailler
  Director - VCSCB Informatics
• Pam Uttz
  Administrative Assistant III

Contact Information

9465 MRB-IV
2213 Garland Avenue
Nashville, TN 37232
United States

Pam Uttz
615-322-7006 (p)
615-322-6645 (f)
Email

Keywords & MeSH Terms

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