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TIFAB Regulates USP15-Mediated p53 Signaling during Stressed and Malignant Hematopoiesis

Cell Rep. 2020;

Niederkorn M, Hueneman K, Choi K, Varney ME, Romano L, Pujato MA, Greis KD, Inoue JI, Meetei R, Starczynowski DT.

Products/Services Used	Details	Operation
Gene Synthesis	e1–e6, February 25, 2020 e1 Continued REAGENT or RESOURCE SOURCE IDENTIFIER USP15 puriﬁed recombinant protein Life Sensors Cat# DB513 USP7 puriﬁed recombinant protein Life Sensors Cat# DB502 IQF di-Ubiquitin substrate (K48) Life Sensors Cat# DU4802 IQF di-ubiquitin substrate (K63) Life Sensors Cat# DU6302 di-Ubiquitin puriﬁed protein panel (K6, K11, K27, K29, K33, K48, K63, M0) Life Sensors Cat# SI200 Recombinant buffer – ‘‘Mock’’ Genscript, This study N/A DUB assay buffer This study N/A Tandem-afﬁnity puriﬁcation trition lysis buffer Singh et al.... Recombinant TIFAB proteins Full-length recombinant TIFAB and domain-deletion mutant DNA sequences were generated by Genscript.	Get A Quote

摘要

TRAF-interacting protein with a forkhead-associated domain B (TIFAB) is implicated in myeloid malignancies with deletion of chromosome 5q. Employing a combination of proteomic and genetic approaches, we find that TIFAB regulates ubiquitin-specific peptidase 15 (USP15) ubiquitin hydrolase activity. Expression of TIFAB in hematopoietic stem/progenitor cells (HSPCs) permits USP15 signaling to substrates, including MDM2 and KEAP1, and mitigates p53 expression. Consequently, TIFAB-deficient HSPCs exhibit compromised USP15 signaling and are sensitized to hematopoietic stress by derepression of p53. In MLL-AF9 leukemia, deletion of TIFAB increases p53 signaling and correspondingly decreases leukemic cell function and... More