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LC–MS/MS Proteomic Profiling of PEAK3 S69 Phosphorylation in PEAK3 Mutants

ABSTRACT: This project aims to investigate how different PEAK3 mutations affect phosphorylation at serine 69 (S69). To this end, we performed proteomic analyses on immunoprecipitated (IP) PEAK3 samples from both wild-type and mutant constructs. Peptides containing phosphorylated and non-phosphorylated S69 were specifically identified and compared to assess mutation-dependent changes in S69 phosphorylation.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Changyuan Hu

LAB HEAD: Roger J. Daly

PROVIDER: PXD071947 | Pride | 2026-03-16

REPOSITORIES: Pride

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			Action	DRS
	Human_reviewedOnly_iRT_20200325-PEAK3mut.fasta	Fasta
	L551.raw	Raw
	L551_-45.mzxml	Mzxml
	L551_-65.mzxml	Mzxml
	L552.raw	Raw

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Publications

A tandem recruitment site in the pseudokinase scaffold PEAK3 is subject to phosphorylation-dependent regulation and cancer-associated mutations.

Zhao Tianyue T Hou Jianmei J Hu Changyuan C Cotton Thomas R TR Daly Roger J RJ

The Journal of biological chemistry 20260310 5

The PEAK protein family, comprising PEAK1-3, are pseudokinase scaffolds that regulate cell proliferation and motility via recruitment of specific effectors. For PEAK3, the latter include the adaptor proteins Grb2 and CrkII and the Arf GTPase-activating protein (ArfGAP) ASAP1. PEAK3 exhibits a tandem site spanning a CrkII SH3 domain binding sequence and phosphorylation-dependent 14-3-3 recruitment motif at serine 69 (S69), with 14-3-3 binding mediating a negative control 'switch' on PEAK3 signali ...[more]

PMID: 41819264

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