BiographyAlan Mullen, MD, PhD is an Assistant Professor of Medicine at Harvard Medical School, Assistant in Medicine at MGH and a member of the MGH Liver Center.
Dr. Mullen's clinical interests are focused on treating patients with chronic liver disease including patients who have progressed to liver fibrosis and cirrhosis. In his practice he cares for patients with conditions including hepatitis A, hepatitis B and hepatitis C, non-alcoholic fatty liver disease (NAFLD), autoimmune hepatitis, cholestatic liver disease including primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) as well as inherited conditions including hemochromatosis and alpha-1-antitrypsin deficiency. He also evaluates patients for abnormal liver function tests and abnormal liver imaging. Dr Mullen also performs endoscopies including diagnostic and therapeutic upper endoscopies and colonoscopies.
ResearchTGF-beta signaling regulates diverse process from normal development, wound healing and tissue homeostasis to tumor formation, hepatic fibrosis and metastasis. The TGF-beta signaling pathway is mediated through activation of Smad2 and Smad3, which are proteins that bind DNA in association with other transcription factors to regulate gene expression. Numerous different cell types in the body respond to TGF-beta signaling, but each cell type has a different response. We have found that key transcription factors that are required to determine cell identity also act to direct Smad transcription factors to their target genes. This association provided a mechanism for TGF-beta signaling to regulate genes most relevant to a specific cell type.
My laboratory uses a combined approach of genomics, genetics and biochemistry to study how TGF-beta signaling regulates early embryonic differentiation by controlling both coding and non-coding genes. We also apply the tools we have developed in studying early development to understand how TGF-beta signaling regulates expression of coding and non-coding genes in hepatic fibrosis with the goal of developing approaches to inhibit or reverse fibrosis.
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