Proteomics

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IP-MS of DCAF1/VprBP interacting proteins in mouse CD4 T cells

ABSTRACT: DCAF1, also known as VprBP (HIV-1-viral-protein-r-binding-protein), is an evolutionary conserved substrate-binding subunit of CRL4 (Cul4a-Ddb1-Roc1) ubiquitin ligase complex. It is a cellular protein targeted by HIV-1 viral protein R (Vpr). DCAF1 modulates cellular response against HIV in macrophages, controls the survival and reprogramming of oocyte, and regulates G2/M transition. DCAF1 functions through diverse mechanisms including regulating protein poly-ubiquitination, mono-ubiquitination and phosphorylation. Nonetheless, whether and how DCAF1 controls the function of primary T cell, a major cell type infected by HIV, remains unknown. We found DCAF1 is required for cell size growth and cell cycle entry from quiescence. To investigate the underlying molecular mechanisms and identify the cellular factors that associate with DCAF1 in T cells, we analyzed DCAF1-interacting proteins in T cells using VprBP immunoprecipitation and mass spectrometry.

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Spleen, T Cell, Lymph Node

SUBMITTER: Yisong Wan  

LAB HEAD: Yisong Y. Wan

PROVIDER: PXD003180 | Pride | 2016-01-12

REPOSITORIES: Pride

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Publications

DCAF1 controls T-cell function via p53-dependent and -independent mechanisms.

Guo Zengli Z   Kong Qing Q   Liu Cui C   Zhang Song S   Zou Liyun L   Yan Feng F   Whitmire Jason K JK   Xiong Yue Y   Chen Xian X   Wan Yisong Y YY  

Nature communications 20160105

On activation, naive T cells grow in size and enter cell cycle to mount immune response. How the fundamental processes of T-cell growth and cell cycle entry are regulated is poorly understood. Here we report that DCAF1 (Ddb1-cullin4-associated-factor 1) is essential for these processes. The deletion of DCAF1 in T cells impairs their peripheral homeostasis. DCAF1 is upregulated on T-cell receptor activation and critical for activation-induced T-cell growth, cell cycle entry and proliferation. In  ...[more]

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