| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Binhua P Zhou, Mien-Chie Hun. Novel targets of Akt, p21(Cipl/WAF1), and MDM2. Seminars in oncology. vol 29. issue 3 Suppl 11. 2002-08-14. PMID:12138399. |
the recent identification of a number of akt substrates suggests that akt can enhance cell proliferation and inhibit apoptosis. |
2002-08-14 |
2023-08-12 |
human |
| Binhua P Zhou, Mien-Chie Hun. Novel targets of Akt, p21(Cipl/WAF1), and MDM2. Seminars in oncology. vol 29. issue 3 Suppl 11. 2002-08-14. PMID:12138399. |
in this review we will discuss the theme of action of akt in regulating the cellular localization of its substrates to control proliferation and apoptosis in light of two new identified akt substrates, p21(cip1/waf1) and mdm2. |
2002-08-14 |
2023-08-12 |
human |
| Andrew Xiao, Hua Wu, Pier Paolo Pandolfi, David N Louis, Terry Van Dyk. Astrocyte inactivation of the pRb pathway predisposes mice to malignant astrocytoma development that is accelerated by PTEN mutation. Cancer cell. vol 1. issue 2. 2002-08-13. PMID:12086874. |
using a conditional allele of t(121), early lethality was circumvented, and adult mice developed high-grade astrocytoma, in which regions of decreased apoptosis expressed activated akt. |
2002-08-13 |
2023-08-12 |
mouse |
| Sreenivasa R Chinni, Fazlul H Sarka. Akt inactivation is a key event in indole-3-carbinol-induced apoptosis in PC-3 cells. Clinical cancer research : an official journal of the American Association for Cancer Research. vol 8. issue 4. 2002-08-12. PMID:11948137. |
akt inactivation is a key event in indole-3-carbinol-induced apoptosis in pc-3 cells. |
2002-08-12 |
2023-08-12 |
human |
| Sreenivasa R Chinni, Fazlul H Sarka. Akt inactivation is a key event in indole-3-carbinol-induced apoptosis in PC-3 cells. Clinical cancer research : an official journal of the American Association for Cancer Research. vol 8. issue 4. 2002-08-12. PMID:11948137. |
a cell survival pathway involving phosphatidylinositol 3'-kinase (pi3k) and akt is known to play an important role in inhibiting apoptosis in response to growth factor signaling, which prompted us to investigate whether this pathway plays any role in i3c-induced apoptosis in pca cells. |
2002-08-12 |
2023-08-12 |
human |
| Sreenivasa R Chinni, Fazlul H Sarka. Akt inactivation is a key event in indole-3-carbinol-induced apoptosis in PC-3 cells. Clinical cancer research : an official journal of the American Association for Cancer Research. vol 8. issue 4. 2002-08-12. PMID:11948137. |
from these results, we conclude that i3c-induced apoptosis is partly mediated by the inhibition of akt activation, resulting in the alterations in the downstream regulatory molecules of akt activation in pc-3 cells. |
2002-08-12 |
2023-08-12 |
human |
| Maria Chiara Deregibus, Vincenzo Cantaluppi, Sophie Doublier, Maria Felice Brizzi, Ilaria Deambrosis, Adriana Albini, Giovanni Camuss. HIV-1-Tat protein activates phosphatidylinositol 3-kinase/ AKT-dependent survival pathways in Kaposi's sarcoma cells. The Journal of biological chemistry. vol 277. issue 28. 2002-08-12. PMID:11994280. |
experiments with a function blocking anti-vascular endothelial cell growth factor receptor-2 antibody suggested that both the early and delayed akt activation and the protection from apoptosis were triggered by the interaction of tat with vascular endothelial cell growth factor receptor-2. |
2002-08-12 |
2023-08-12 |
Not clear |
| Ming-Jen Hsu, Shiuh-Sheng Lee, Wan-Wan Li. Polysaccharide purified from Ganoderma lucidum inhibits spontaneous and Fas-mediated apoptosis in human neutrophils through activation of the phosphatidylinositol 3 kinase/Akt signaling pathway. Journal of leukocyte biology. vol 72. issue 1. 2002-08-12. PMID:12101282. |
western blotting indicates the stimulating effect of ps-g on akt phosphorylation and its inhibition of procaspase 3 degradation, which occurs in neutrophils undergoing spontaneous apoptosis or triggered death by fas. |
2002-08-12 |
2023-08-12 |
human |
| Wen-Hua Zheng, Satyabrata Kar, Rémi Quirio. Insulin-like growth factor-1-induced phosphorylation of transcription factor FKHRL1 is mediated by phosphatidylinositol 3-kinase/Akt kinase and role of this pathway in insulin-like growth factor-1-induced survival of cultured hippocampal neurons. Molecular pharmacology. vol 62. issue 2. 2002-08-05. PMID:12130673. |
fkhrl1, a member of the forkhead family of transcription factors possibly involved in cell cycle and apoptosis, is a downstream target of akt in fibroblasts. |
2002-08-05 |
2023-08-12 |
Not clear |
| Eva Tomás, Yen-Shou Lin, Zeina Dagher, Asish Saha, Zhijun Luo, Yasuo Ido, Neil B Ruderma. Hyperglycemia and insulin resistance: possible mechanisms. Annals of the New York Academy of Sciences. vol 967. 2002-08-02. PMID:12079834. |
here, it was associated with an increased propensity to apoptosis and, as in muscle, with an impaired ability of insulin to activate akt. |
2002-08-02 |
2023-08-12 |
human |
| Jiayuh Lin, Huaijing Tang, Xiaohong Jin, Guiyue Jia, Jer-Tsong Hsie. p53 regulates Stat3 phosphorylation and DNA binding activity in human prostate cancer cells expressing constitutively active Stat3. Oncogene. vol 21. issue 19. 2002-07-29. PMID:12082540. |
interestingly, p53-dependent apoptosis occurred in the presence of high levels of phosphorylated akt and erk1/2 in both du145 and tsu prostate cancer cells. |
2002-07-29 |
2023-08-12 |
human |
| Takashi Matsui, Ling Li, Justina C Wu, Stuart A Cook, Tomohisa Nagoshi, Michael H Picard, Ronglih Liao, Anthony Rosenzwei. Phenotypic spectrum caused by transgenic overexpression of activated Akt in the heart. The Journal of biological chemistry. vol 277. issue 25. 2002-07-19. PMID:11943770. |
the serine-threonine kinase, akt, inhibits cardiomyocyte apoptosis acutely both in vitro and in vivo. |
2002-07-19 |
2023-08-12 |
mouse |
| Gwendolyn S Kerby, Vincent Cottin, Frank J Accurso, Fukun Hoffmann, Edward D Chan, Valerie A Fadok, David W H Riche. Impairment of macrophage survival by NaCl: implications for early pulmonary inflammation in cystic fibrosis. American journal of physiology. Lung cellular and molecular physiology. vol 283. issue 1. 2002-07-19. PMID:12060576. |
because the activation of p42(mapk/erk2) and akt has been associated with survival responses, we investigated the effect of nacl on macrophage apoptosis. |
2002-07-19 |
2023-08-12 |
mouse |
| Gwendolyn S Kerby, Vincent Cottin, Frank J Accurso, Fukun Hoffmann, Edward D Chan, Valerie A Fadok, David W H Riche. Impairment of macrophage survival by NaCl: implications for early pulmonary inflammation in cystic fibrosis. American journal of physiology. Lung cellular and molecular physiology. vol 283. issue 1. 2002-07-19. PMID:12060576. |
collectively, these findings indicate that modest elevations in nacl differentially regulate the activation of mitogen-activated protein kinases and akt and potentiate macrophage apoptosis. |
2002-07-19 |
2023-08-12 |
mouse |
| Ho-Young Lee, Kyung-Hee Chun, Bingrong Liu, Sandra A Wiehle, Richard J Cristiano, Waun Ki Hong, Pinchas Cohen, Jonathan M Kuri. Insulin-like growth factor binding protein-3 inhibits the growth of non-small cell lung cancer. Cancer research. vol 62. issue 12. 2002-07-19. PMID:12068000. |
transient transfection with activated akt or constitutively active mapk kinase-1, an upstream activator of mapk, partially blocked igfbp-3-induced apoptosis of nsclc cells. |
2002-07-19 |
2023-08-12 |
mouse |
| David R Plas, Craig B Thompso. Cell metabolism in the regulation of programmed cell death. Trends in endocrinology and metabolism: TEM. vol 13. issue 2. 2002-07-16. PMID:11854022. |
here, we review the coordinated effects of growth factor withdrawal on bioenergetics and programmed cell death, and discuss the metabolic consequences of genes that prevent apoptosis, including the bcl2 family of genes and akt. |
2002-07-16 |
2023-08-12 |
Not clear |
| Agnieszka Bronisz, Barbara Gajkowska, Krystyna Domańska-Jani. PKC and Raf-1 inhibition-related apoptotic signalling in N2a cells. Journal of neurochemistry. vol 81. issue 6. 2002-07-12. PMID:12068066. |
we present evidence that, in the absence of serum in the medium, decreased phosphorylation of raf-1 and bad112, as well as akt and bad136, proteins and their translocation to mitochondria coincided with sts10 - or wm-induced apoptosis, respectively. |
2002-07-12 |
2023-08-12 |
Not clear |
| Kan Kageyama, Yoshito Ihara, Shinji Goto, Yoshishige Urata, Genji Toda, Katsusuke Yano, Takahito Kond. Overexpression of calreticulin modulates protein kinase B/Akt signaling to promote apoptosis during cardiac differentiation of cardiomyoblast H9c2 cells. The Journal of biological chemistry. vol 277. issue 22. 2002-07-02. PMID:11907032. |
thus, overexpression of calreticulin promotes differentiation-dependent apoptosis in h9c2 cells by suppressing the akt signaling pathway. |
2002-07-02 |
2023-08-12 |
mouse |
| Kan Kageyama, Yoshito Ihara, Shinji Goto, Yoshishige Urata, Genji Toda, Katsusuke Yano, Takahito Kond. Overexpression of calreticulin modulates protein kinase B/Akt signaling to promote apoptosis during cardiac differentiation of cardiomyoblast H9c2 cells. The Journal of biological chemistry. vol 277. issue 22. 2002-07-02. PMID:11907032. |
these findings indicate a novel mechanism by which cytoplasmic akt signaling is modulated to cause apoptosis by a resident protein of the endoplasmic reticulum, calreticulin. |
2002-07-02 |
2023-08-12 |
mouse |
| Kouji Tsugawa, Michael K Jones, Keizo Sugimachi, I James Sarfeh, Andrzej S Tarnawsk. Biological role of phosphatase PTEN in cancer and tissue injury healing. Frontiers in bioscience : a journal and virtual library. vol 7. 2002-06-28. PMID:11991859. |
pten can: 1) inhibit entry into the cell cycle by inhibiting g1 to s phase progression and arrest cell proliferation required for tissue reconstruction during injury healing; 2) increase apoptosis by blocking akt activation leading to increased bad and caspase-9 activities; 3) inhibit hypoxia-induced angiogenesis required for injury healing by blocking akt-mediated vegf gene transcription; 4) inhibit akt-mediated cell migration, i.e. |
2002-06-28 |
2023-08-12 |
Not clear |