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Cited by 421

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

The BAD protein integrates survival signaling by EGFR/MAPK and PI3K/Akt kinase pathways in PTEN-deficient tumor cells

Open access
She, Qing-Bai, Solit, David B., Ye, Qing, O’Reilly, Kathryn E., Lobo, Jose, Rosen, Neal·2005·Cancer Cell

Abstract

Tumor cells with mutated PTEN proliferate in an EGFR-independent manner. Induction of PTEN sensitizes cells to EGFR inhibition, and the combination causes synergistic apoptosis. Synergy is due to inhibition of two parallel pathways that phosphorylate the proapoptotic protein BAD at distinct sites. Serine 112 phosphorylation is EGFR/MEK/MAPK dependent, whereas serine 136 phosphorylation is PI3K/Akt dependent. Either phosphorylation is sufficient to sequester BAD to 14-3-3. BAD is released and apoptosis is induced only if both serines are dephosphorylated in response to inhibition of both pathways. Reduction of BAD expression by RNA interference prevents apoptosis in response to pathway inhibition. Thus, BAD integrates the antiapoptotic effects of both pathways. Combined inhibition of EGFR and PI3K signaling may be a useful therapeutic strategy.

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Metadata

Authors
She, Q.-B., Solit, D. B., Ye, Q., O’Reilly, K. E., Lobo, J., & Rosen, N.
Venue
Cancer Cell
Publisher
Elsevier BV
Published
2005-10
Volume
8
Issue
4
Pages
287-297
ISSN
1535-6108 (ISSN-L)
OpenAlex
W2122624068
Cited by
421
References
3
FWCI
11.29
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: The BAD protein integrates survival signaling by EGFR/MAPK and PI3K/Akt kinase pathways in PTEN-deficient tumor cells. https://app.cochat.ai/papers/10.1016/j.ccr.2005.09.006
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She, Q.-B., Solit, D. B., Ye, Q., O’Reilly, K. E., Lobo, J., & Rosen, N. (2005). The BAD protein integrates survival signaling by EGFR/MAPK and PI3K/Akt kinase pathways in PTEN-deficient tumor cells. Cancer Cell. https://doi.org/10.1016/j.ccr.2005.09.006

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