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Phosphorylation of Bcl-xL by ERK1

ABSTRACT: The anti-apoptotic function of Bcl-xL in the heart against reperfusion injury is diminished by K-Ras-Mst1-mediated phosphorylation of Ser14, which allows dissociation of Bcl-xL from Bax and promotes cardiomyocyte death. Here we show that Ser14 phosphorylation of Bcl-xL is also promoted by hemodynamic stress in the heart, through the H-Ras-ERK pathway. Our study suggests that phosphorylation of Bcl-xL at Ser14 in response to acute pressure overload plays an essential role in mediating compensatory hypertrophy by promoting calcium release, alleviating the negative constraint of Bcl-xL upon the IP3R-NFAT pathway.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human)

DISEASE(S): Cardiovascular System Disease

SUBMITTER: Michinari Nakamura

LAB HEAD: Michinari Nakamura

PROVIDER: PXD045118 | Pride | 2023-09-06

REPOSITORIES: Pride

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			Action	DRS
	Michi_lane2_ERK1.mgf	Mgf
	Michi_lane2_ERK1.mzML	Mzml
	Michi_lane2_ERK1.mzid.gz	Mzid
	Michi_lane2_ERK1.raw	Raw
	checksum.txt	Txt

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