Zobrazeno 1 - 10
of 10
pro vyhledávání: '"Prashanth T. Bhaskar"'
Autor:
Wan-Ni Yu, Veronique Nogueira, Arya Sobhakumari, Krushna C. Patra, Prashanth T. Bhaskar, Nissim Hay
Publikováno v:
Cell Reports, Vol 12, Iss 4, Pp 610-621 (2015)
Akt is frequently activated in human cancers. However, it is unknown whether systemic inhibition of a single Akt isoform could regress cancer progression in cancers that are not driven by Akt activation. We systemically deleted Akt1 after tumor onset
Externí odkaz:
https://doaj.org/article/fbd2c6be520f4c5db88c47b7ad95aca1
Autor:
Gopalakrishnan Ramakrishnan, Alexandre Ferro Aissa, Rho H, Sang-Min Jeon, Robey Rb, Prashanth T. Bhaskar, Maxim V. Frolov, Krushna C. Patra, Nissim Hay, Nogueira, Catherine Blaha, Soeun Kang, Alexander R. Terry
Hexokinase 2 (HK2), a glycolytic enzyme that catalyzes the first committed step in glucose metabolism, is markedly induced in cancer cells. HK2’s role in tumorigenesis has been attributed to its glucose kinase activity. However, we uncovered a nove
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::c8966f3dd7bce4517995971e56624f43
https://doi.org/10.1101/2021.04.08.439049
https://doi.org/10.1101/2021.04.08.439049
Autor:
Sang-Min Jeon, Prashanth T. Bhaskar, Brooks R.B. Robey, Alexander R. Terry, Hyunsoo Rho, Nissim Hay, Catherine Blaha, Soeun Kang, Gopalakrishnan Ramakrishnan, Alexandre Ferro Aissa, Maxim V. Frolov, Veronique Nogueira, Krushna C. Patra
Publikováno v:
SSRN Electronic Journal.
Hexokinase 2 (HK2), a glycolytic enzyme that catalyzes the first committed step in glucose metabolism, is markedly induced in cancer cells. HK2’s role in tumorigenesis has been attributed to its glucose kinase activity. However, we uncovered a nove
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::d9ea99d956aa937dc6955cedb1277e16
https://doi.org/10.2139/ssrn.3864441
https://doi.org/10.2139/ssrn.3864441
Autor:
Prashanth T. Bhaskar, Arya Sobhakumari, Wan Ni Yu, Krushna C. Patra, Veronique Nogueira, Nissim Hay
Publikováno v:
Cell Reports, Vol 12, Iss 4, Pp 610-621 (2015)
Summary Akt is frequently activated in human cancers. However, it is unknown whether systemic inhibition of a single Akt isoform could regress cancer progression in cancers that are not driven by Akt activation. We systemically deleted Akt1 after tum
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::bfe87d96d773eb2e575b3ffde0ea2c35
http://www.sciencedirect.com/science/article/pii/S221112471500683X
http://www.sciencedirect.com/science/article/pii/S221112471500683X
Autor:
Veronique Nogueira, Sang-Min Jeon, Prashanth T. Bhaskar, R. Brooks Robey, Krushna C. Patra, Young-Kyu Park, Nissim Hay
Publikováno v:
Molecular and Cellular Biology. 29:5136-5147
The current concept is that Tsc-deficient cells are sensitized to apoptosis due to the inhibition of Akt activity by the negative feedback mechanism induced by the hyperactive mTORC1. Unexpectedly, however, we found that Tsc1/2-deficient cells exhibi
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7c16544b722adb5701470e38fb460cf7
https://doi.org/10.1128/mcb.01946-08
https://doi.org/10.1128/mcb.01946-08
Autor:
Prashanth T. Bhaskar, Nissim Hay
Publikováno v:
Developmental Cell. 12:487-502
The regulatory circuits that control the activities of the two distinct target of rapamycin (TOR) complexes, TORC1 and TORC2, and of Akt have been a focus of intense research in recent years. It has become increasingly evident that these regulatory c
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a7d1107e03015dcb614c7120d35e3752
https://doi.org/10.1016/j.devcel.2007.03.020
https://doi.org/10.1016/j.devcel.2007.03.020
Autor:
Xiao Ding Peng, Prashanth T. Bhaskar, Hiroaki Kiyokawa, Nissim Hay, Annett Hahn-Windgassen, Chia Chen Chen, Veronique Nogueira, Jennifer E. Skeen, William S. Chen
Publikováno v:
Cancer cell. 10(4)
SummaryAkt contributes to tumorigenesis by inhibiting apoptosis. Here we establish that Akt is required for normal cell proliferation and susceptibility to oncogenesis independently of its antiapoptotic activity. Partial ablation of Akt activity by d
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::49065f78a80f8d09bbf2ded62778605f
https://pubmed.ncbi.nlm.nih.gov/17045203
https://pubmed.ncbi.nlm.nih.gov/17045203
Autor:
Kathrin Gottlob, R. Brooks Robey, Jennifer E. Skeen, Nathan Majewski, Veronique Nogueira, Navdeep S. Chandel, Platina E. Coy, Prashanth T. Bhaskar, Craig B. Thompson, Nissim Hay
Publikováno v:
Molecular cell. 16(5)
The serine/threonine kinase Akt inhibits mitochondrial cytochrome c release and apoptosis induced by a variety of proapoptotic stimuli. The antiapoptotic activity of Akt is coupled, at least in part, to its effects on cellular metabolism. Here, we pr
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::83224bb1284c52215012bd1df4b3defa
https://pubmed.ncbi.nlm.nih.gov/15574336
https://pubmed.ncbi.nlm.nih.gov/15574336
Autor:
Markku Laakso, Gromoslaw A. Smolen, Eric L. Allen, Abhishek K. Jha, Qi Wang, Luke L. Miller, Prashanth T. Bhaskar, Krushna C. Patra, Zebin Wang, Nissim Hay, R. Brooks Robey, Navdeep S. Chandel, Michelle Clasquin, William J. Muller, Will Wheaton
Publikováno v:
Cancer Cell. (2):213-228
SummaryAccelerated glucose metabolism is a common feature of cancer cells. Hexokinases catalyze the first committed step of glucose metabolism. Hexokinase 2 (HK2) is expressed at high level in cancer cells, but only in a limited number of normal adul
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e985f25c4b45f1218e3a3f41dc2405ea
Autor:
Deepa Sundararajan, Young-Kyu Park, Ivana Tonic, Veronique Nogueira, Nissim Hay, Sang-Min Jeon, Chia Chen Chen, Prashanth T. Bhaskar
Publikováno v:
Developmental Cell. (4):592-604
FoxO transcription factors and TORC1 are conserved downstream effectors of Akt. Here we unraveled regulatory circuits underlying interplay between Akt, FoxO, and mTOR. Activated FoxO1 inhibits mTORC1 by TSC2-dependent and TSC2-independent mechanisms.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::47ab8d46800a6bc24fc1f7cd16274ec4