Zobrazeno 1 - 10
of 20
pro vyhledávání: '"John S. Coukos"'
Autor:
Benjamin D. Stein, John R. Ferrarone, Eric E. Gardner, Jae Won Chang, David Wu, Pablo E. Hollstein, Roger J. Liang, Min Yuan, Qiuying Chen, John S. Coukos, Miriam Sindelar, Bryan Ngo, Steven S. Gross, Reuben J. Shaw, Chen Zhang, John M. Asara, Raymond E. Moellering, Harold Varmus, Lewis C. Cantley
Publikováno v:
Cancer Discovery. 13:1002-1025
KRAS is the most frequently mutated oncogene in human lung adenocarcinomas (hLUAD), and activating mutations frequently co-occur with loss-of-function mutations in TP53 or STK11/LKB1. However, mutation of all three genes is rarely observed in hLUAD,
Publikováno v:
ACS Chemical Biology. 18:91-101
Methylglyoxal (MGO), a reactive metabolite byproduct of glucose metabolism, is known to form a variety of posttranslational modifications (PTMs) on nucleophilic amino acids. For example, cysteine, the most nucleophilic proteinogenic amino acid, forms
Autor:
Thomas E. Speltz, Zeyu Qiao, Colin S. Swenson, Xianghang Shangguan, John S. Coukos, Christopher W. Lee, Deborah M. Thomas, Jesse Santana, Sean W. Fanning, Geoffrey L. Greene, Raymond E. Moellering
Publikováno v:
Nature Biotechnology. 41:541-551
Autor:
Lewis C. Cantley, Harold Varmus, Raymond E. Moellering, John M. Asara, Chen Zhang, Reuben J. Shaw, Steven S. Gross, Bryan Ngo, Miriam Sindelar, John S. Coukos, Qiuying Chen, Min Yuan, Roger J. Liang, Pablo E. Hollstein, David Wu, Jae Won Chang, Eric E. Gardner, John R. Ferrarone, Benjamin D. Stein
Figure S7. Tpi1 is required for tumor growth in KP and KPL LUAD models.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::222d1f5d233f06829de0b48c421cb0f7
https://doi.org/10.1158/2159-8290.22553374
https://doi.org/10.1158/2159-8290.22553374
Autor:
Lewis C. Cantley, Harold Varmus, Raymond E. Moellering, John M. Asara, Chen Zhang, Reuben J. Shaw, Steven S. Gross, Bryan Ngo, Miriam Sindelar, John S. Coukos, Qiuying Chen, Min Yuan, Roger J. Liang, Pablo E. Hollstein, David Wu, Jae Won Chang, Eric E. Gardner, John R. Ferrarone, Benjamin D. Stein
Figure S8. Tpi1 inactivation in KL autochthonous tumor model alters histology and pathology.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3ef35cef9249e7becb510aad36608db4
https://doi.org/10.1158/2159-8290.22553371.v1
https://doi.org/10.1158/2159-8290.22553371.v1
Autor:
Lewis C. Cantley, Harold Varmus, Raymond E. Moellering, John M. Asara, Chen Zhang, Reuben J. Shaw, Steven S. Gross, Bryan Ngo, Miriam Sindelar, John S. Coukos, Qiuying Chen, Min Yuan, Roger J. Liang, Pablo E. Hollstein, David Wu, Jae Won Chang, Eric E. Gardner, John R. Ferrarone, Benjamin D. Stein
Figure S6. TPI1 allelic variants effects central carbon metabolic flux.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6aeb978252524d78cdce8afd4f13fcfa
https://doi.org/10.1158/2159-8290.22553377
https://doi.org/10.1158/2159-8290.22553377
Autor:
Lewis C. Cantley, Harold Varmus, Raymond E. Moellering, John M. Asara, Chen Zhang, Reuben J. Shaw, Steven S. Gross, Bryan Ngo, Miriam Sindelar, John S. Coukos, Qiuying Chen, Min Yuan, Roger J. Liang, Pablo E. Hollstein, David Wu, Jae Won Chang, Eric E. Gardner, John R. Ferrarone, Benjamin D. Stein
KRAS is the most frequently mutated oncogene in human lung adenocarcinomas (hLUAD), and activating mutations frequently co-occur with loss-of-function mutations in TP53 or STK11/LKB1. However, mutation of all three genes is rarely observed in hLUAD,
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::74a4888ce7db00a4ab236f555bdd0a96
https://doi.org/10.1158/2159-8290.c.6534613.v2
https://doi.org/10.1158/2159-8290.c.6534613.v2
Autor:
Lewis C. Cantley, Harold Varmus, Raymond E. Moellering, John M. Asara, Chen Zhang, Reuben J. Shaw, Steven S. Gross, Bryan Ngo, Miriam Sindelar, John S. Coukos, Qiuying Chen, Min Yuan, Roger J. Liang, Pablo E. Hollstein, David Wu, Jae Won Chang, Eric E. Gardner, John R. Ferrarone, Benjamin D. Stein
Figure S3. TPI1 phosphorylation regulates triose phosphate levels and metabolic flux.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0e442f21632c30fbcd19a65b226840d4
https://doi.org/10.1158/2159-8290.22553386
https://doi.org/10.1158/2159-8290.22553386
Autor:
Lewis C. Cantley, Harold Varmus, Raymond E. Moellering, John M. Asara, Chen Zhang, Reuben J. Shaw, Steven S. Gross, Bryan Ngo, Miriam Sindelar, John S. Coukos, Qiuying Chen, Min Yuan, Roger J. Liang, Pablo E. Hollstein, David Wu, Jae Won Chang, Eric E. Gardner, John R. Ferrarone, Benjamin D. Stein
Figure S5. LKB1 regulates the multimeric state of hTPI1 but not mTpi1 and substitution of Cys in hTPI1 causes formation of a covalent TPI1 dimer.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4ef4602a6ebc5d3aa9748829c925ec2e
https://doi.org/10.1158/2159-8290.22494733.v1
https://doi.org/10.1158/2159-8290.22494733.v1
Autor:
Lewis C. Cantley, Harold Varmus, Raymond E. Moellering, John M. Asara, Chen Zhang, Reuben J. Shaw, Steven S. Gross, Bryan Ngo, Miriam Sindelar, John S. Coukos, Qiuying Chen, Min Yuan, Roger J. Liang, Pablo E. Hollstein, David Wu, Jae Won Chang, Eric E. Gardner, John R. Ferrarone, Benjamin D. Stein
Figure S2. Phosphorylation of human TPI1 is LKB1-dependent.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5edbac7dd14f6886e6e25d88b0a60582
https://doi.org/10.1158/2159-8290.22494742.v1
https://doi.org/10.1158/2159-8290.22494742.v1