| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Haiyun Ling, Tong Zhang, Laetitia Pereira, Christopher Kable Means, Hongqiang Cheng, Yusu Gu, Nancy D Dalton, Kirk L Peterson, Ju Chen, Donald Bers, Joan Heller Brown, Joan Heller Brow. Requirement for Ca2+/calmodulin-dependent kinase II in the transition from pressure overload-induced cardiac hypertrophy to heart failure in mice. The Journal of clinical investigation. vol 119. issue 5. 2009-06-08. PMID:19381018. |
strikingly, while ko mice showed preserved hypertrophy after 6-week tac, camkiidelta deficiency significantly ameliorated phenotypic changes associated with the transition to heart failure, such as chamber dilation, ventricular dysfunction, lung edema, cardiac fibrosis, and apoptosis. |
2009-06-08 |
2023-08-12 |
mouse |
| Etsuo Susaki, Keiko Nakayama, Lili Yamasaki, Keiichi I Nakayam. Common and specific roles of the related CDK inhibitors p27 and p57 revealed by a knock-in mouse model. Proceedings of the National Academy of Sciences of the United States of America. vol 106. issue 13. 2009-05-07. PMID:19276117. |
such developmental defects of p57(ko) mice were also ameliorated in mice deficient in both p57 and the transcription factor e2f1, suggesting that loss of p57 promotes e2f1-dependent apoptosis. |
2009-05-07 |
2023-08-12 |
mouse |
| Takahiro Nakayama, Waichi Sato, Tomoki Kosugi, Li Zhang, Martha Campbell-Thompson, Ashio Yoshimura, Byron P Croker, Richard J Johnson, Takahiko Nakagaw. Endothelial injury due to eNOS deficiency accelerates the progression of chronic renal disease in the mouse. American journal of physiology. Renal physiology. vol 296. issue 2. 2009-03-30. PMID:19036847. |
renal injuries in the rk-enos ko mice were accompanied by a greater loss of endothelial cells that was shown to be due to both a decrease in endothelial cell proliferation and an increase in apoptosis. |
2009-03-30 |
2023-08-12 |
mouse |
| Luisa Riccardi, Emanuela Mazzon, Stefano Bruscoli, Emanuela Esposito, Concetta Crisafulli, Rosanna Di Paola, Rocco Caminiti, Carlo Riccardi, Salvatore Cuzzocre. Peroxisome proliferator-activated receptor-alpha modulates the anti-inflammatory effect of glucocorticoids in a model of inflammatory bowel disease in mice. Shock (Augusta, Ga.). vol 31. issue 3. 2009-03-19. PMID:18665053. |
in particular, dex was less effective in ppar-[alpha]ko compared with wt mice, as evaluated by inhibition of proinflammatory cytokines production, cell migration, oxidative stress, apoptosis, and colon injury. |
2009-03-19 |
2023-08-12 |
mouse |
| Vellareddy Anantharam, Arthi Kanthasamy, Christopher J Choi, Dustin P Martin, Calivarathan Latchoumycandane, Jüergen A Richt, Anumantha G Kanthasam. Opposing roles of prion protein in oxidative stress- and ER stress-induced apoptotic signaling. Free radical biology & medicine. vol 45. issue 11. 2009-02-03. PMID:18835352. |
interestingly, er stress-induced activation of caspases, pkcdelta, and apoptosis was significantly exacerbated in prp(c) cells, whereas h(2)o(2)-induced proapoptotic changes were suppressed in prp(c) compared to prp(ko) cells. |
2009-02-03 |
2023-08-12 |
Not clear |
| Xiaoqing He, Hong Kan, Lu Cai, Qiang M. Nrf2 is critical in defense against high glucose-induced oxidative damage in cardiomyocytes. Journal of molecular and cellular cardiology. vol 46. issue 1. 2009-02-03. PMID:19007787. |
concomitantly, high glucose induced significantly higher levels of apoptosis at lower concentrations and in shorter time in nrf2 ko cells than in wt cells. |
2009-02-03 |
2023-08-12 |
mouse |
| Xiaoqing He, Hong Kan, Lu Cai, Qiang M. Nrf2 is critical in defense against high glucose-induced oxidative damage in cardiomyocytes. Journal of molecular and cellular cardiology. vol 46. issue 1. 2009-02-03. PMID:19007787. |
additionally, cardiomyocytes from nrf2 ko mice exhibited increased sensitivity to 3-nitropropionic acid, an inhibitor of mitochondrial respiratory complex ii, for both ros production and apoptosis compared with nrf2 wt cells, further emphasizing the role of nrf2 in ros defense in the cells. |
2009-02-03 |
2023-08-12 |
mouse |
| Ann M Toth, Patricia Devaux, Roberto Cattaneo, Charles E Samue. Protein kinase PKR mediates the apoptosis induction and growth restriction phenotypes of C protein-deficient measles virus. Journal of virology. vol 83. issue 2. 2009-01-26. PMID:19004947. |
furthermore, infection with wt, v(ko), or especially c(ko) virus caused significantly less apoptosis in pkr(kd) cells than in pkr-sufficient cells. |
2009-01-26 |
2023-08-12 |
human |
| Ann M Toth, Patricia Devaux, Roberto Cattaneo, Charles E Samue. Protein kinase PKR mediates the apoptosis induction and growth restriction phenotypes of C protein-deficient measles virus. Journal of virology. vol 83. issue 2. 2009-01-26. PMID:19004947. |
although apoptosis induced by c(ko) virus infection in pkr-sufficient cells was blocked by a caspase antagonist, the growth of c(ko) virus was not restored to the wt level by treatment with this pharmacologic inhibitor. |
2009-01-26 |
2023-08-12 |
human |
| Kevin Larade, Zhigang Jiang, Yongzhao Zhang, WenFang Wang, Susan Bonner-Weir, Hao Zhu, H Franklin Bun. Loss of Ncb5or results in impaired fatty acid desaturation, lipoatrophy, and diabetes. The Journal of biological chemistry. vol 283. issue 43. 2008-12-11. PMID:18682384. |
treatment of ko hepatocytes with palmitic acid reduced cell viability and increased apoptosis, a response blunted by co-incubation with oleic acid. |
2008-12-11 |
2023-08-12 |
mouse |
| Charles H Rundle, Xiaoguang Wang, Matilda H-C Sheng, Jon E Wergedal, K-H William Lau, Subburaman Moha. Bax deficiency in mice increases cartilage production during fracture repair through a mechanism involving increased chondrocyte proliferation without changes in apoptosis. Bone. vol 43. issue 5. 2008-12-02. PMID:18708175. |
tunel analysis showed no significant differences in the number of either chondrocyte or non-chondrocyte apoptotic cells between bax ko and c57bl/6j fractures at 7 or 14 days post-fracture, indicating that the increased number of chondrocytes in bax ko fractures was not due to reduced apoptosis. |
2008-12-02 |
2023-08-12 |
mouse |
| Charles H Rundle, Xiaoguang Wang, Matilda H-C Sheng, Jon E Wergedal, K-H William Lau, Subburaman Moha. Bax deficiency in mice increases cartilage production during fracture repair through a mechanism involving increased chondrocyte proliferation without changes in apoptosis. Bone. vol 43. issue 5. 2008-12-02. PMID:18708175. |
analysis of expression of apoptotic genes revealed that although the expression levels of bcl-2 and bcl-xl were not different between the bax ko and c57bl/6j mice at 7 or 14 days post-fracture, the expression of bh3-domain only bak and "bik-like" pro-apoptotic gene increased approximately 1.5-fold and approximately 2-fold, respectively, in bax ko fractures at 7 and 14 days post-fracture, compared to c57bl/6j fractures, suggesting that up-regulation of the bak and bik-like pro-apoptotic genes in bax ko mice might compensate for the lack of bax functions in the context of apoptosis. |
2008-12-02 |
2023-08-12 |
mouse |
| Charles H Rundle, Xiaoguang Wang, Matilda H-C Sheng, Jon E Wergedal, K-H William Lau, Subburaman Moha. Bax deficiency in mice increases cartilage production during fracture repair through a mechanism involving increased chondrocyte proliferation without changes in apoptosis. Bone. vol 43. issue 5. 2008-12-02. PMID:18708175. |
in conclusion, this study demonstrates for the first time that bax has an important role in the early stage of fracture healing, and that the increased callus size and cartilage area in bax ko fractures was due to increased chondrocyte proliferation and not to reduced apoptosis or increased chondrocyte hypertrophy. |
2008-12-02 |
2023-08-12 |
mouse |
| Sanjay Pradhan, Hee Kyung Kim, Christopher J Thrash, Maureen A Cox, Sudheer K Mantena, Jian-He Wu, Mohammad Athar, Santosh K Katiyar, Craig A Elmets, Laura Timare. A critical role for the proapoptotic protein bid in ultraviolet-induced immune suppression and cutaneous apoptosis. Journal of immunology (Baltimore, Md. : 1950). vol 181. issue 5. 2008-09-15. PMID:18713978. |
we have shown that lcs derived from mice deficient in the proapoptotic bid (bh3-interacting death domain protein) gene (bid ko) resist apoptosis and induce amplified immune responses. |
2008-09-15 |
2023-08-12 |
mouse |
| Yuko Sato, Takashi Baba, Mohamad Zubair, Kanako Miyabayashi, Yoshiro Toyama, Mamiko Maekawa, Akiko Owaki, Hirofumi Mizusaki, Tatsuya Sawamura, Kiyotaka Toshimori, Ken-Ichirou Morohashi, Yuko Katoh-Fuku. Importance of forkhead transcription factor Fkhl18 for development of testicular vasculature. Molecular reproduction and development. vol 75. issue 9. 2008-09-09. PMID:18288644. |
these gaps probably represented ectopic apoptosis of testicular periendothelial cells, identified by caspase-3 expression, in ko fetuses. |
2008-09-09 |
2023-08-12 |
mouse |
| Yuko Sato, Takashi Baba, Mohamad Zubair, Kanako Miyabayashi, Yoshiro Toyama, Mamiko Maekawa, Akiko Owaki, Hirofumi Mizusaki, Tatsuya Sawamura, Kiyotaka Toshimori, Ken-Ichirou Morohashi, Yuko Katoh-Fuku. Importance of forkhead transcription factor Fkhl18 for development of testicular vasculature. Molecular reproduction and development. vol 75. issue 9. 2008-09-09. PMID:18288644. |
considering that fas ligand gene expression is activated by foxs, the elevated activity of foxs in the absence of fkhl18 probably explains the marked apoptosis of periendothelial cells in fkhl18 ko mice. |
2008-09-09 |
2023-08-12 |
mouse |
| Siobhán C Cowley, Michael F Goldberg, J Anthony Ho, Karen L Elkin. The membrane form of tumor necrosis factor is sufficient to mediate partial innate immunity to Francisella tularensis live vaccine strain. The Journal of infectious diseases. vol 198. issue 2. 2008-08-13. PMID:18593295. |
by day 6 after infection, tnf ko mice, but not memtnf mice, exhibited massive apoptosis in spleens and livers, which shortly preceded their death. |
2008-08-13 |
2023-08-12 |
mouse |
| Siobhán C Cowley, Michael F Goldberg, J Anthony Ho, Karen L Elkin. The membrane form of tumor necrosis factor is sufficient to mediate partial innate immunity to Francisella tularensis live vaccine strain. The Journal of infectious diseases. vol 198. issue 2. 2008-08-13. PMID:18593295. |
thus, memtnf partially functions to regulate chemokine expression, cell recruitment, and nitric oxide production during primary lvs infection and protects against the induction of apoptosis observed in tnf ko mice. |
2008-08-13 |
2023-08-12 |
mouse |
| Kristi L Norris, Richard J Youl. Cytomegalovirus proteins vMIA and m38.5 link mitochondrial morphogenesis to Bcl-2 family proteins. Journal of virology. vol 82. issue 13. 2008-08-06. PMID:18417572. |
consistently with bax-selective inactivation by m38.5, m38.5 fragments mitochondria in bak knockout (ko) cells and protects bak ko cells from apoptosis better than bax ko cells. |
2008-08-06 |
2023-08-12 |
human |
| Tomasz P Rygiel, Alexander E Mertens, Kristin Strumane, Rob van der Kammen, John G Collar. The Rac activator Tiam1 prevents keratinocyte apoptosis by controlling ROS-mediated ERK phosphorylation. Journal of cell science. vol 121. issue Pt 8. 2008-08-05. PMID:18349077. |
previously, we found that tiam1 knockout (ko) mice are resistant to dmba-induced skin tumorigenicity, which correlated with increased apoptosis in keratinocytes of the skin epidermis. |
2008-08-05 |
2023-08-12 |
mouse |