Proteomics

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A549 overexpressing CCAR1 LC-MS/MS

ABSTRACT: CCAR1 mRNA have two transcripts, the 3.5 kb full length transcript and the 2.5 kb shorter transcript which contained a deletion in exon 15—exon 22 of full-length CCAR1 cDNA, where sequences mapped to 1196–3120 bp were missed. CCAR1L and CCAR1S shared a common N-terminus and a common C-terminal end, but the latter had a deletion of SAP domain. As a DNA/RNA-binding domain, the SAP motif is involved in chromosomal organization and apoptosis. To explaine the divergence of CCAR1L and CCAR1S in regulating apoptosis,we purified CCAR1L and CCAR1S from flag-CCAR1L or CCAR1S overexpressing A549 cells by performing IP-MS to screening the possible proteins which are specifically interacting with CCAR1L or CCAR1S.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Polycystic Kidney,Disease Free

SUBMITTER: Huang Qingyang  

LAB HEAD: Zhang Lingqiang

PROVIDER: PXD009266 | Pride | 2018-05-15

REPOSITORIES: pride

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0000_service_ZhangLingqiang_180302_HF5_CZH_human_L_50per_F1_R1.raw Raw
0000_service_ZhangLingqiang_180302_HF5_CZH_human_S_50per_F1_R1.raw Raw
0000_service_ZhangLingqiang_180302_HF5_CZH_human_V_50per_F1_R1.raw Raw
F001741_l_pepxml.xml Xml
F001742_s_pepxml.xml Xml
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Publications

Mutually exclusive acetylation and ubiquitylation of the splicing factor SRSF5 control tumor growth.

Chen Yuhan Y   Huang Qingyang Q   Liu Wen W   Zhu Qiong Q   Cui Chun-Ping CP   Xu Liang L   Guo Xing X   Wang Ping P   Liu Jingwen J   Dong Guanglong G   Wei Wenyi W   Liu Cui Hua CH   Feng Zhichun Z   He Fuchu F   Zhang Lingqiang L  

Nature communications 20180625 1

Most tumor cells take up more glucose than normal cells. Splicing dysregulation is one of the molecular hallmarks of cancer. However, the role of splicing factor in glucose metabolism and tumor development remains poorly defined. Here, we show that upon glucose intake, the splicing factor SRSF5 is specifically induced through Tip60-mediated acetylation on K125, which antagonizes Smurf1-mediated ubiquitylation. SRSF5 promotes the alternative splicing of CCAR1 to produce CCAR1S proteins, which pro  ...[more]

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