Kirsten Sadler Edepli
- ASSISTANT PROFESSOR Medicine, Liver Diseases
- ASSISTANT PROFESSOR Developmental and Regenerative Biology
B.A., Mount Holyoke College
Biology and Anthropology
M.M.Sc., Harvard Medical School
Markey Scholar Program
Ph.D., Harvard University
Cell and Developmental Biology
fellowship, Massachusetts Institute of Technology
Liver development and regeneration in zebrafish, Nancy Hopkins Laboratory
- Our laboratory studies liver development, fatty liver disease and liver cancer using zebrafish. For detailed information, please consult our lab website.
The Sadler laboratory belongs to:
The Department of Developmental and Regenerative Biology
The Department of Medicine/Division of Liver Diseases
The Mount Sinai Alcoholic Liver Disease Research Center
Training areas in Development and Stem Cell Biology, Cancer Biology and Genetics and Genomics
The Mount Sinai Zebrafish Facility is managed by Dr. Sadler.
Harold and Golden Lamport Award
Mount Sinai School of Medicine
2008 - 2011
Basil O'Connor Starter Scholar Award
March of Dimes
2008 - 2011
Research Scholar Award
American Gastroenterological Association
Dr. Sadler-Edepli is the Director of the Zebrafish Models of Liver Disease Laboratory and the Model Co-Core Director of the Mount Sinai Alcoholic Liver Disease Research Center.
Specific Clinical/Research Interest: Using zebrafish to understand liver development, regeneration and disease.
Students: Raksha Mudbhary, Vinitha Jacob, Brandon Kent (co-mentored with Dr. Martin Walsh)
Postdoctoral Fellows: Deanna Howarth, Ana Vacaru, Orkhontuya Tsedensodnom, Yelena Chernyavskaya
Research Personnel: Evan Closser (Zebrafish Facility manager)
Faculty: Jaime Chu, M.D.
Current Research Focus
Using zebrafish to understand liver development, regeneration and disease
Zebrafish are an excellent model for studying embryonic development and we are using the power of zebrafish genetics to define genes required for liver growth as well as to identify new models of liver diseases. Fatty liver disease is emerging as an important liver pathology and is typically associated with obesity and type II diabetes and together these comprise Metabolic Syndrome, which affects nearly 5 percent of the American population. We have found a zebrafish mutant that develops fatty liver disease in the embryo, and have named it foie gras (foiegr). The foie gras gene is well conserved in animals, and has recently been shown to be a component of the TRAPP complex (trappc11) which functions to tether vesicles in the secretory pathway to their destination compartment. We found that there is significant activation of the unfolded protein response (UPR) in foigr/trappc11 mutants and that in zebrafish, as in mammals, robust UPR induction is sufficient to cause fatty liver disease. Research in the Sadler Edepli lab focuses on understanding the relationship between UPR activation and fatty liver disease, understanding the cellular function of foiegr/trappc11, and using the zebrafish bearing a mutation in the foiegr gene as a model for studying fatty liver disease.
The second focus of our lab is to determine the genetic basis for liver growth in the embryo and during regeneration in adults, and is aimed at testing the hypothesis that a similarprogram may be responsible for growth control in both circumstances. We have carried out a screen to identify zebrafish mutant embryos which fail to undergo liver growth and are testing the genes responsible for the embryonic phenotype for their role in liver regeneration following partial hepatectomy.
Current Research Studies
- Investigating the role of the unfolded protein response in fatty liver disease
- Identifying the pathways required for to steatosis due to acute alcohol exposure.
- Elucidating the cellular function of Foigr/Trappc11.
- Understanding the role of UHRF1 in liver growth, regeneration and liver cancer.
- Determining how UHRF1 is regulated by phosphorylation.
Chu J, Mir A, Gao N, Rosa S, Monson C, Sharma V, Steet R, Freeze HH, Lehrman MA, Sadler KC. A zebrafish model of congenital disorders of glycosylation with phosphomannose isomerase deficiency reveals an early opportunity for corrective mannose supplementation. Disease models & mechanisms 2013 Jan; 6(1).
Imrie D, Sadler KC. Stress management: How the unfolded protein response impacts fatty liver disease. Journal of hepatology 2012 Nov; 57(5).
Howarth DL, Vacaru AM, Tsedensodnom O, Mormone E, Nieto N, Costantini LM, Snapp EL, Sadler KC. Alcohol disrupts endoplasmic reticulum function and protein secretion in hepatocytes. Alcoholism, clinical and experimental research 2012 Jan; 36(1).
Cinaroglu A, Gao C, Imrie D, Sadler KC. Activating transcription factor 6 plays protective and pathological roles in steatosis due to endoplasmic reticulum stress in zebrafish. Hepatology (Baltimore, Md.) 2011 Aug; 54(2).
Passeri M, Cinaroglu A, Gao C, Sadler KC. Hepatic Steatosis in Response to Acute Alcohol Exposure in Zebrafish Depends Upon SREBP Activation. Hepatology 2008; 49.
Chu J, Sadler KC. New school in liver development: lessons from zebrafish [review]. Hepatology (Baltimore, Md.) 2009 Nov; 50(5).
Imrie D, Sadler KC. White adipose tissue development in zebrafish is regulated by both developmental time and fish size. Developmental Dynamics 2010; 239(11): 3013-.
Chu J, Loughlin EA, Gaur NA, SenBanerjee S, Jacob V, Monson C, Kent B, Oranu A, Ding Y, Ukomadu C, Sadler KC. UHRF1 phosphorylation by cyclin A2/cyclin-dependent kinase 2 is required for zebrafish embryogenesis. Molecular biology of the cell 2012 Jan; 23(1).
Tien AL, Senbanerjee S, Kulkarni A, Mudbhary R, Goudreau B, Ganesan S, Sadler KC, Ukomadu C. UHRF1 depletion causes a G2/M arrest, activation of DNA damage response and apoptosis. The Biochemical journal 2011 Apr; 435(1).
Zhao X, Monson C, Gao C, Gouon-Evans V, Matsumoto N, Sadler KC, Friedman SL. Klf6/copeb is required for hepatic outgrowth in zebrafish and for hepatocyte specification in mouse ES cells. Developmental biology 2010 Aug; 344(1).
Sadler KC, Krahn KN, Gaur NA, Ukomadu C. Liver growth in the embryo and during liver regeneration in zebrafish requires the cell cycle regulator, uhrf1. Proc Natl Acad Sci U S A 2007; 104: 1570-1575.
Physicians and scientists on the faculty of the Icahn School of Medicine at Mount Sinai often interact with pharmaceutical, device and biotechnology companies to improve patient care, develop new therapies and achieve scientific breakthroughs. In order to promote an ethical and transparent environment for conducting research, providing clinical care and teaching, Mount Sinai requires that salaried faculty inform the School of their relationships with such companies.
Dr. Sadler Edepli did not report having any of the following types of financial relationships with industry during 2012 and/or 2013: consulting, scientific advisory board, industry-sponsored lectures, service on Board of Directors, participation on industry-sponsored committees, equity ownership valued at greater than 5% of a publicly traded company or any value in a privately held company. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.
Mount Sinai's faculty policies relating to faculty collaboration with industry are posted on our website at http://icahn.mssm.edu/about-us/services-and-resources/faculty-resources/handbooks-and-policies/faculty-handbook. Patients may wish to ask their physician about the activities they perform for companies.
Annenberg Building Floor 25 Room 25-26B (office); 30 (lab)
1468 Madison Avenue
New York, NY 10029
Annenberg Building Floor 25 Room 25-30 (lab);
1468 Madison Avenue
New York, NY 10029