Loss of the Tumor Suppressor BAP1 Causes Myeloid Transformation | Zendy

Anwesha Dey | Zendy; Dhaya Seshasayee | Zendy; Rajkumar Noubade | Zendy; Dorothy French | Zendy; Jinfeng Liu | Zendy; Mira S. Chaurushiya | Zendy; Donald S. Kirkpatrick | Zendy; Victoria C. Pham | Zendy; Jennie R. Lill | Zendy; Corey E. Bakalarski | Zendy; Jian Wu | Zendy; Lilian Phu | Zendy; Paula Katavolos | Zendy; Lindsay M. LaFave | Zendy; Omar AbdelWahab | Zendy; Zora Modrušan | Zendy; Somasekar Seshagiri | Zendy; Ken C. Dong | Zendy; Zhonghua Lin | Zendy; Mercedesz Balázs | Zendy; Rowena Suriben | Zendy; Kim Newton | Zendy; S.G. Hymowitz | Zendy; Guillermo GarciaManero | Zendy; Flavius Martin | Zendy; Ross L. Levine | Zendy; Vishva M. Dixit | Zendy

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Loss of the Tumor Suppressor BAP1 Causes Myeloid Transformation

Author(s) -

Anwesha Dey,

Dhaya Seshasayee,

Rajkumar Noubade,

Dorothy French,

Jinfeng Liu,

Mira S. Chaurushiya,

Donald S. Kirkpatrick,

Victoria C. Pham,

Jennie R. Lill,

Corey E. Bakalarski,

Jian Wu,

Lilian Phu,

Paula Katavolos,

Lindsay M. LaFave,

Omar AbdelWahab,

Zora Modrušan,

Somasekar Seshagiri,

Ken C. Dong,

Zhonghua Lin,

Mercedesz Balázs,

Rowena Suriben,

Kim Newton,

S.G. Hymowitz,

Guillermo GarciaManero,

Flavius Martin,

Ross L. Levine,

Vishva M. Dixit

Publication year - 2012

Publication title -

science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 12.556

H-Index - 1186

eISSN - 1095-9203

pISSN - 0036-8075

DOI - 10.1126/science.1221711

Subject(s) - bap1 , cancer research , chronic myelomonocytic leukemia , biology , loss function , epigenetics , germline mutation , somatic cell , mutation , phenocopy , malignant transformation , myelodysplastic syndromes , gene , genetics , melanoma , immunology , phenotype , bone marrow

De-ubiquitinating enzyme BAP1 is mutated in a hereditary cancer syndrome with increased risk of mesothelioma and uveal melanoma. Somatic BAP1 mutations occur in various malignancies. We show that mouse Bap1 gene deletion is lethal during embryogenesis, but systemic or hematopoietic-restricted deletion in adults recapitulates features of human myelodysplastic syndrome (MDS). Knockin mice expressing BAP1 with a 3xFlag tag revealed that BAP1 interacts with host cell factor-1 (HCF-1), O-linked N-acetylglucosamine transferase (OGT), and the polycomb group proteins ASXL1 and ASXL2 in vivo. OGT and HCF-1 levels were decreased by Bap1 deletion, indicating a critical role for BAP1 in stabilizing these epigenetic regulators. Human ASXL1 is mutated frequently in chronic myelomonocytic leukemia (CMML) so an ASXL/BAP1 complex may suppress CMML. A BAP1 catalytic mutation found in a MDS patient implies that BAP1 loss of function has similar consequences in mice and humans.

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