| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| K H Limesand, K A Barzen, D O Quissell, S M Anderso. Synergistic suppression of apoptosis in salivary acinar cells by IGF1 and EGF. Cell death and differentiation. vol 10. issue 3. 2003-12-12. PMID:12700634. |
igf1 significantly suppressed etoposide-induced apoptosis, measured by caspase 3 activation and quantitation of cellular subg(1) dna content, in rat parotid salivary acinar cells (c5). |
2003-12-12 |
2023-08-12 |
rat |
| K H Limesand, K A Barzen, D O Quissell, S M Anderso. Synergistic suppression of apoptosis in salivary acinar cells by IGF1 and EGF. Cell death and differentiation. vol 10. issue 3. 2003-12-12. PMID:12700634. |
transduction of c5 cells with an adenovirus expressing a constitutively activated mutant of akt-suppressed etoposide-induced apoptosis, whereas a kinase-inactive mutant of akt suppressed the protective effect of igf1. |
2003-12-12 |
2023-08-12 |
rat |
| b' Pavel Haninec, Ladislav Houst\'ava, Lubom\\xc3\\xadr Stejskal, Petr Dubov\\xc3\\xb. Rescue of rat spinal motoneurons from avulsion-induced cell death by intrathecal administration of IGF-I and Cerebrolysin. Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft. vol 185. issue 3. 2003-07-07. PMID:12801087.' |
we have found that avulsion of the c5 ventral roots results in significant loss of motoneurons in the same spinal cord segment due mainly to apoptosis. |
2003-07-07 |
2023-08-12 |
rat |
| Bart De Vries, Robert A Matthijsen, Tim G A M Wolfs, Annemarie A J H M Van Bijnen, Peter Heeringa, Wim A Buurma. Inhibition of complement factor C5 protects against renal ischemia-reperfusion injury: inhibition of late apoptosis and inflammation. Transplantation. vol 75. issue 3. 2003-03-20. PMID:12589162. |
inhibition of complement factor c5 protects against renal ischemia-reperfusion injury: inhibition of late apoptosis and inflammation. |
2003-03-20 |
2023-08-12 |
Not clear |
| J L Hirpara, M V Clément, S Pervai. Intracellular acidification triggered by mitochondrial-derived hydrogen peroxide is an effector mechanism for drug-induced apoptosis in tumor cells. The Journal of biological chemistry. vol 276. issue 1. 2001-02-08. PMID:11016925. |
we recently showed that two photoproducts of merocyanine 540, c2 and c5, triggered cytochrome c release; however, c5 was inefficient in inducing caspase activity and apoptosis in leukemia cells, unlike c2. |
2001-02-08 |
2023-08-12 |
Not clear |
| L Smith, L Chen, M E Reyland, T A DeVries, R V Talanian, S Omura, J B Smit. Activation of atypical protein kinase C zeta by caspase processing and degradation by the ubiquitin-proteasome system. The Journal of biological chemistry. vol 275. issue 51. 2001-02-01. PMID:11016947. |
induction of apoptosis in rat parotid c5 cells produced catalytic domain polypeptides of endogenous pkczeta and increased pkczeta activity. |
2001-02-01 |
2023-08-12 |
human |
| S Umeoka, O Miyamoto, N A Janjua, S Nagao, T Itan. Appearance and alteration of TUNEL positive cells through epileptogenesis in amygdaloid kindled rat. Epilepsy research. vol 42. issue 2-3. 2000-12-20. PMID:11074182. |
the present data showed that in the course of getting the epileptogenesis, apoptosis had already occurred and this type of cell death may play a significant role in reaching stage c5 through kindling. |
2000-12-20 |
2023-08-12 |
rat |
| S M Dashiell, H Rus, C L Kosk. Terminal complement complexes concomitantly stimulate proliferation and rescue of Schwann cells from apoptosis. Glia. vol 30. issue 2. 2000-04-27. PMID:10719360. |
the consequences of sublytic terminal complement complex (tcc) assembly on schwann cell proliferation and apoptosis were examined by using purified complement proteins (c5*-9) or antibody-sensitized schwann cells in the presence of a serum that was depleted of the seventh component of complement (c7dhs) and reconstituted with purified c7. |
2000-04-27 |
2023-08-12 |
Not clear |
| S M Dashiell, H Rus, C L Kosk. Terminal complement complexes concomitantly stimulate proliferation and rescue of Schwann cells from apoptosis. Glia. vol 30. issue 2. 2000-04-27. PMID:10719360. |
sublytic c5*-9 significantly inhibited apoptosis 41% by 24 h, as determined by a terminal deoxyuridine triphosphate-biotin nick end labeling assay, and also decreased annexin-v binding at 4 h. collectively, these data suggest that sublytic tcc, like beta-nrg, is a potent schwann cell trophic factor that is capable of stimulating mitogenesis and apoptotic rescue. |
2000-04-27 |
2023-08-12 |
Not clear |
| J L Hirpara, M A Seyed, K W Loh, H Dong, R M Kini, S Pervai. Induction of mitochondrial permeability transition and cytochrome C release in the absence of caspase activation is insufficient for effective apoptosis in human leukemia cells. Blood. vol 95. issue 5. 2000-03-29. PMID:10688837. |
thus, we demonstrate that mpt induction and cytochrome c release by the novel compound c5, in the absence of effective caspase activation, is insufficient for triggering efficient apoptosis in tumor cells. |
2000-03-29 |
2023-08-12 |
human |
| S M Anderson, M E Reyland, S Hunter, L M Deisher, K A Barzen, D O Quissel. Etoposide-induced activation of c-jun N-terminal kinase (JNK) correlates with drug-induced apoptosis in salivary gland acinar cells. Cell death and differentiation. vol 6. issue 5. 1999-09-09. PMID:10381634. |
in contrast to the parotid c5 cells, the vast majority of submandibular c6 cells appeared to be resistant to etoposide-induced apoptosis. |
1999-09-09 |
2023-08-12 |
rat |
| S M Anderson, M E Reyland, S Hunter, L M Deisher, K A Barzen, D O Quissel. Etoposide-induced activation of c-jun N-terminal kinase (JNK) correlates with drug-induced apoptosis in salivary gland acinar cells. Cell death and differentiation. vol 6. issue 5. 1999-09-09. PMID:10381634. |
etoposide induced apoptosis in the parotid c5 cell line as evidenced by the appearance of cytoplasmic blebbing and nuclear condensation, dna fragmentation and cleavage of parp. |
1999-09-09 |
2023-08-12 |
rat |
| S M Anderson, M E Reyland, S Hunter, L M Deisher, K A Barzen, D O Quissel. Etoposide-induced activation of c-jun N-terminal kinase (JNK) correlates with drug-induced apoptosis in salivary gland acinar cells. Cell death and differentiation. vol 6. issue 5. 1999-09-09. PMID:10381634. |
these data suggest that etoposide may induce apoptosis in parotid c5 cells by activating jnks and suppressing the activation of erks, thus creating an imbalance in these two signaling pathways. |
1999-09-09 |
2023-08-12 |
rat |
| M E Reyland, S M Anderson, A A Matassa, K A Barzen, D O Quissel. Protein kinase C delta is essential for etoposide-induced apoptosis in salivary gland acinar cells. The Journal of biological chemistry. vol 274. issue 27. 1999-07-27. PMID:10383415. |
we have previously shown that parotid c5 salivary acinar cells undergo apoptosis in response to etoposide treatment as indicated by alterations in cell morphology, caspase-3 activation, dna fragmentation, sustained activation of c-jun n-terminal kinase, and inactivation of extracellular regulated kinases 1 and 2. |
1999-07-27 |
2023-08-12 |
Not clear |
| E Takashita, K Sugimoto, Y Adachi, Y Aihara, H Inoue, H Jiang, T Katakai, K J Mor. Destruction of hematopoietic microenvironment by cytotoxic T cells. Experimental hematology. vol 25. issue 10. 1997-10-01. PMID:9293900. |
these data suggest that the aforementioned factors mediate induction of apoptosis in ms-5 cells induced by direct cell-to-cell interaction with stil-3 c5. |
1997-10-01 |
2023-08-12 |
mouse |
| R Geffen, R S Goldstei. Rescue of sensory ganglia that are programmed to degenerate in normal development: evidence that NGF modulates proliferation of DRG cells in vivo. Developmental biology. vol 178. issue 1. 1997-04-14. PMID:8812108. |
since growth factors modulate both proliferation and apoptosis, we postulated that these molecules and/or their receptors might be responsible for the difference in fate between c2 and c5. |
1997-04-14 |
2023-08-12 |
chicken |