Celastrol inhibits tumor cell proliferation and promotes apoptosis through the activation of c-Jun N-terminal kinase and suppression of PI3 K/Akt signaling pathways (Q39501449)

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English	Celastrol inhibits tumor cell proliferation and promotes apoptosis through the activation of c-Jun N-terminal kinase and suppression of PI3 K/Akt signaling pathways	scientific article

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scholarly article

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Europe PubMed Central

12 September 2017

Celastrol inhibits tumor cell proliferation and promotes apoptosis through the activation of c-Jun N-terminal kinase and suppression of PI3 K/Akt signaling pathways (English)

1 reference

Europe PubMed Central

12 September 2017

apoptotic process

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author name string

Radhamani Kannaiyan

1

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Europe PubMed Central

12 September 2017

Kanjoormana Aryan Manu

2

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Europe PubMed Central

12 September 2017

Luxi Chen

3

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Europe PubMed Central

12 September 2017

Feng Li

4

1 reference

Europe PubMed Central

12 September 2017

Peramaiyan Rajendran

5

1 reference

Europe PubMed Central

12 September 2017

Aruljothi Subramaniam

6

1 reference

Europe PubMed Central

12 September 2017

Paula Lam

7

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Europe PubMed Central

12 September 2017

Alan Prem Kumar

8

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Europe PubMed Central

12 September 2017

Gautam Sethi

9

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Europe PubMed Central

12 September 2017

publication date

1 October 2011

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Europe PubMed Central

12 September 2017

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Europe PubMed Central

12 September 2017

16

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Europe PubMed Central

12 September 2017

10

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Europe PubMed Central

12 September 2017

1028-1041

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Europe PubMed Central

12 September 2017

https://scigraph.springernature.com/pub.10.1007/s10495-011-0629-6

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Celastrol, a triterpene extracted from the Chinese "Thunder of God Vine," is a potent proteasome inhibitor and suppresses human prostate cancer growth in nude mice

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Celastrol, a novel HSP90 inhibitor, depletes Bcr-Abl and induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation

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Celastrol suppresses angiogenesis-mediated tumor growth through inhibition of AKT/mammalian target of rapamycin pathway

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Exploring death receptor pathways as selective targets in cancer therapy

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Apoptosis signaling

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Phorbol esters induce death in MCF-7 breast cancer cells with altered expression of protein kinase C isoforms. Role for p53-independent induction of gadd-45 in initiating death.

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The NF-kappaB-mediated control of the JNK cascade in the antagonism of programmed cell death in health and disease

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Identification of beta-escin as a novel inhibitor of signal transducer and activator of transcription 3/Janus-activated kinase 2 signaling pathway that suppresses proliferation and induces apoptosis in human hepatocellular carcinoma cells.

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Colony-stimulating factor 1 regulates novel cyclins during the G1 phase of the cell cycle

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Formation and activation of a cyclin E-cdk2 complex during the G1 phase of the human cell cycle

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Curcumin induces the degradation of cyclin E expression through ubiquitin-dependent pathway and up-regulates cyclin-dependent kinase inhibitors p21 and p27 in multiple human tumor cell lines

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JNK signaling in apoptosis

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Cell-cycle inhibition by independent CDK and PCNA binding domains in p21Cip1

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Identifiers

10.1007/S10495-011-0629-6

1 reference

Europe PubMed Central

12 September 2017

release_wohdaopkivgizizged3prlm4nu

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1 reference

Europe PubMed Central

12 September 2017

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