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Willenbring Lab »  Alumni »  Postdoctoral Fellows »  Aras N. Mattis, M.D., Ph.D.
Aras N. Mattis, M.D., Ph.D.

Aras N. Mattis, M.D., Ph.D.

Assistant Professor, UCSF Department of Pathology

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University of California, Berkeley, B.A., Molecular and Cell Biology, 1998

University of Illinois, Chicago, M.D., Medicine, 2007

University of Illinois, Urbana-Champaign, Ph.D., Biochemistry, 2007

University of California, San Francisco, Anatomic Pathology Resident 2007-2009

University of California, San Francisco, Fellow, Surgical Pathology, 2009-2010

University of California, San Francisco, Fellow, Liver/GI Pathology, 2010-Present

  • American Board of Pathology, Anatomic Pathology
  • UCSF Department of Pathology
  • California Institute for Regenerative Medicine
  • Liver and Gastrointestinal Pathology
  • Development and metabolism, liver and gastrointestinal tumors, site-specific recombination.
  • Hepatocytes for transplant and disease modeling, micro-RNA regulation of hepatocyte
  • Liver diseases including metabolic, pediatric, fibrotic, idiopathic, stem cell derived

Aras N. Mattis, M.D., Ph.D., is a board-certified anatomic pathologist and clinical fellow in the Willenbring Lab. Dr. Mattis trained at the University of Illinois at Urbana-Champaign, earning both his doctorates, Biochemistry and Medicine, there in 2007. He continued his clinical training in Pathology at the University of California San Francisco completing residency in Anatomic Pathology with subsequent fellowship training in Surgical Pathology and Liver and gastrointestinal pathology under his clinical mentor, Dr. Linda Ferrell. Since 2010, he has worked in the Willenbring Lab, investigating the basic mechanisms of liver development and disease in the with a specific focus on liver metabolism and fatty liver disease as well as micro-RNA regulation of liver metabolism.

Dr. Mattis' postdoctoral work includes the use of translational human biopsy material as well as patient-derived induced pluripotent stem cell reprogramming to hepatocytes. As a long-term goal, this work aims to develop a humanized liver mouse model of fatty liver disease. Aras is supported by the UCSF CIRM clinical fellow training grant and continues to work closely with the UCSF Department of Pathology as a clinical researcher.

Data provided by UCSF Profiles, powered by CTSI
  • Regulation of Lipid Metabolism by miR-29a within Hepatocytes
    Sponsor:
    Sponsor ID:
    Funding Period:
    Sep 2013
    -
    Jul 2018
    Principal Investigator
MOST RECENT PUBLICATIONS FROM A TOTAL OF 30
Data provided by UCSF Profiles, powered by CTSI
  1. Alsamman S, Christenson SA, Yu A, Ayad NME, Mooring MS, Segal JM, Hu JK, Schaub JR, Ho SS, Rao V, Marlow MM, Turner SM, Sedki M, Pantano L, Ghoshal S, Ferreira DDS, Ma HY, Duwaerts CC, Espanol-Suner R, Wei L, Newcomb B, Mileva I, Canals D, Hannun YA, Chung RT, Mattis AN, Fuchs BC, Tager AM, Yimlamai D, Weaver VM, Mullen AC, Sheppard D, Chen JY. Targeting acid ceramidase inhibits YAP/TAZ signaling to reduce fibrosis in mice. Sci Transl Med. 2020 Aug 19; 12(557). View in PubMed
  2. Alkhani A, Levy CS, Tsui M, Rosenberg KA, Polovina K, Mattis AN, Mack M, Van Dyken S, Wang BM, Maher JJ, Nijagal A. Ly6cLo non-classical monocytes promote resolution of rhesus rotavirus-mediated perinatal hepatic inflammation. Sci Rep. 2020 Apr 28; 10(1):7165. View in PubMed
  3. Wen KW, Rabinovitch PS, Wang D, Mattis AN, Ferrell LD, Choi WT. Utility of DNA flow cytometry in distinguishing between malignant and benign intrahepatic biliary lesions. Virchows Arch. 2020 Apr 15. View in PubMed
  4. Lee H, Rabinovitch PS, Mattis AN, Kakar S, Choi WT. DNA flow cytometric analysis of paraffin-embedded tissue for the diagnosis of malignancy in bile duct biopsies. Hum Pathol. 2020 May; 99:80-87. View in PubMed
  5. Schwab ME, Song H, Mattis A, Phelps A, Vu LT, Huang FW, Nijagal A. De novo somatic mutations and KRAS amplification are associated with cholangiocarcinoma in a patient with a history of choledochal cyst. J Pediatr Surg. 2020 Mar 24. View in PubMed
  6. View All Publications

 

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