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Article

p66Shc-dependent apoptosis requires Lck and CamKII activity.

Apoptosis : an international journal on programmed cell death - 1 Feb 2012

Patrussi Laura, Giommoni Nico, Pellegrini Michela, Gamberucci Alessandra, Baldari Cosima T

Abstract excerpt

p66Shc, an adaptor molecule which enhances reactive oxygen species (ROS) production by mitochondria, promotes T-cell apoptosis by inducing mitochondrial dysfunction and impairing Ca(2+) homeostasis. We have addressed the potential role of Lck, a kinase which has been implicated in T-cell apoptosis induced by a number of stimuli, in the proapoptotic activity of p66Shc. Lck deficiency in Jurkat T cells...

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Identifiers

PMID: 21983898
DOI: 10.1007/s10495-011-0663-4

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

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