Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10415 (Bcl-2)
 33,771 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A novel protein named apoptin induces a p53-independent, Bcl-2 insensitive type apoptosis in various human tumor cells but not in normal cells. Apoptin is considered to be a promising candidate for safe and effective anti-tumortherapy. Moreover, apoptin may be important for fundamental studies on molecularbasis of apoptosis and cancer. Apoptin gene was subcloned into prokaryotic expression vector pPROEXHT and pBV220, respectively. The apoptin protein was obtained from pPROEXHT-apoptin expression system and not from pBV220-apoptin the former contains a 6xhistidine affinity tag for ease of purification. Expressed protein was purified by chromatography on a co-chelated affinity column and was renatured by dialysis. The renatured apoptin was able to induce purified Hela nuclei apoptosis in vitro even without the participation of the cytoplasm, showing that apoptin expressed in E.coli was active to induce apoptosis.
Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai) 2001
PMID:Expression, Purification and in vitro Activity of Apoptin. 1205 Aug 15

Effects of mitochondrial permeability transition pore-specific inhibitor cyclosporine A (CsA) and highly expressed Bcl-2 on the apoptosis of HL-60 cells induced by EGTA were studied. Detection of apoptotic peak by flow cytometry, fluorescent microscope observation of chromatin condensation with double staining of PI and Hoechst33342 and DNA ladder analysis all demonstrated that CsA obviously enhanced the apoptosis of HL-60 cells induced by EGTA, while highly expressed Bcl-2 completely blocked it. It is revealed by mitochondrial membrane potential (deltapsi(m)) fluorescent probes rhodamine 123 and CMXRos that the deltapsi(m) decreased in the apoptosis of HL-60 cells induced by EGTA. CsA enhanced the decrease of deltapsi(m), but highly expressed Bcl-2 increased deltapsi(m) of HL-60 cells about 2-fold and completely blocked the decrease of deltapsi(m).
Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai) 2001
PMID:Effects of Cyclosporine A and Highly Expressed Bcl-2 on Apoptosis of HL-60 Cells Induced by EGTA. 1205 Aug 21

Bcl-2 family proteins play key roles in apoptosis. They coordinate with other apoptotic proteins in apoptosis to control mitochondria stability both in structure and function, while mitochondria probably act as the main switch of apoptosis. Bcl-2 family proteins can be divided into two types, antiapoptotic proteins and pro-apoptotic proteins. During apoptosis, Bcl-2 family proapoptotic proteins can translocate to the outer membrane of mitochondrion after posttranslational modification by certain proteases such as caspases. Then cytochrome c (cyt.c), apoptosis-inducing factors (AIFs), and other proapoptotic factors are released from mitochondrion, triggering apoptosis. Bcl-2 family antiapoptotic proteins sequestered in mitochondrion have ability to inhibit the release of cyt.c and AIFs, and prevent apoptosis. When interacting with activated proapoptotic proteins, the antiapoptotic proteins lose inhibiting ability of pro-apoptotic factors' release, and again triggering apoptosis. Based on the newest research evolvements, types, structures, localizations, apoptosis regulating mechanisms of Bcl-2 family proteins are reviewed.
Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai) 2002 Jul
PMID:Bcl-2 family proteins and apoptosis. 1209 57

Various extracelluar stimulation, including those by growth factors and cytokines, can induce the bcl-2 gene expression. Bcl-2 protein induced by this stimulation seems to be essential for cell survival. In order to understand the regulations of bcl-2 transcription, recent advances at transcriptional and post-transcriptional levels in this field will be described.
Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai) 2000
PMID:Transcription Regulation of bcl-2 Gene. 1209 82

Apoptosis is usually accompanied by DNA fragmentation and up-regulation of reactive oxygen species, and it can be inhibited by overexpression of Bcl-2. Here, cadmium was found to induce apoptosis in BA/F3beta cells. MTT assay, Hochest 33258 staining, and transmission electron microscopy analysis were used to detect the apoptosis, however, neither DNA fragmentation nor up-regulation of reactive oxygen species were observed in this type of apoptosis. Furthermore, Bcl-2 overexpression had no effect on this type of apoptosis. In conclusion, these data suggested that cadmium induced a novel type of apoptosis in BA/F3beta cells.
Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai) 2000
PMID:A Novel Type of Apoptosis Induced by Cadmium in BA/F3beta Cells. 1211 Sep 19

A lot of molecular biological techniques was used to observe the effect of bcl-2 antisence RNA on human gastric cancer cell line SGC7901 and to detect the inducibility and promotion of MT-II promoter. The results showed that MT-II promoter could be activated by the induction with 160 &mgr;mol/L Zn(2+) and the expression of Bcl-2 plays an important role in apoptosis of SGC7901 cells.
Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai) 1999
PMID:Inducible Expression of bcl-2 Antisense RNA Promotes Apoptosis of Human Gastric Cancer Cell Line. 1213 78

To make an initial inquiry into the correlation of development and prognosis with the expression of Bcl-2 protein in endometrial carcinoma, we detected the Bcl-2 protein expression in 40 normal and 60 malignant samples of the endometrium by means of an immunohistochemical technique. We observed that Bcl-2 expression varied with menstrual cycle, becoming stronger in proliferative phase and then declining in secretory phase. Bcl-2 expression in endometrial carcinoma was much weaker than that in normal endometrium, and Bcl-2 was particularly expressed in adenoacanthoma, papillary adenocarcinoma and simple adenocarcinoma. The higher grade and stage were, the stronger Bcl-2 expression was (P < 0.01). In 5 cases of endometrial carcinoma with hyperplastic endometrium, Bcl-2 expression of carcinoma was obviously weaker than that of hyperplastic endometrium. So we conclude that Bcl-2 overexpression may contribute to the formation of hyperplastic endometrium, that obvious reduction of Bcl-2 expression in endometrial carcinoma may promote apoptosis of cells, and that Bcl-2 over-expression may be associated with good prognosis.
Hua Xi Yi Ke Da Xue Xue Bao 1999 Mar
PMID:[A study of Bcl-2 expression in normal endometrium and endometrial carcinoma]. 1220 37

Low dose radiation induces apoptosis and Bcl-2 can inhibit apoptosis induced by a variety of stimuli. The effects and possible mechanisms of Bcl-2 on 4 Gy X-ray-induced apoptosis in Bcl-2 transfected and untransfected cells were studied. The data present here suggested that overexpression of Bcl-2 significantly inhibited X-ray-induced apoptosis in CHO cells within 72 h. Further investigation demonstrated that Bcl-2 prevented the loss of mitochondrial membrane potential (deltapsim) induced by X-ray irradiation. It appears that overexpression of Bcl-2 blocked the ionizing radiation-induced apoptosis. The maintenance of deltapsim plays an important role in the protective mechanism of Bcl-2 on ionizing radiation-induced apoptosis.
Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai) 1997
PMID:Mitochondrial Mechanisms of Bcl-2 on Ionizing Radiation-induced Apoptosis. 1221 90

Activation of G-protein coupled muscarinic acetylcholine receptors and MAPKs/ERK-1/2 has been found to inhibit neural cell apoptosis and promote neural cell survival. Bcl-2 protein family also plays an important role in regulating neural cell apoptosis and survival. However, signaling pathways coupling muscarinic receptors to Bcl-2 family remains to be elucidated. In the present study, it was found that carbachol not only activated MEK/ERK-1/2 signaling pathways, but also increased the expression levels of Bcl-2 and phospho-Bad proteins in human neuroblastoma SH-SY5Y cells. These effects were blocked by a muscarinic receptor antagonist (atropine) and a MEK inhibitor(PD98059) and were significantly attenuated by a Src family kinases inhibitor(PP1) and a PKC inhibitor (bisindolymaleimide-I), but were not influenced by a G(i/o)-uncoupling reagent (pertussin toxin) and a PI-3 kinase inhibitor (wortmannin). Furthermore, carbachol also stimulated Bcl-2 promoter-driven luciferase gene expression in transfected SH-SY5Y cells. Co-transfection of Ras or Raf dominant negative mutants with the pBcl-2-Luc plasmid abolished carbachol s effects. These data suggested that muscarinic acetylcholine receptors regulated the expression of Bcl-2 protein family by Ras-ERK-1/2 signaling pathway involving the pertussin toxin-insensitive G-proteins, PKC and Src.
Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai) 2003 Jan
PMID:[G-protein-coupled muscarinic acetylcholine receptor activation up-regulates Bcl-2 and phospho-bad via Ras-ERK-1/2 signaling pathway]. 1251 26

This study was aimed at the level and implication of expression of c-myb and bcl-2 proteins in C6 glioma. The therapeutic effect of oncogene c-myb antisense oligodeoxynucleotide on C6 glioma in nude mice was studied. C6 glioma cells were implanted into the cutis of 36 nude mice. Ten days later, the nude mice were randomly divided into three groups and were treated with SON, AON and normal saline respectively. Three mice of every group were killed at 4 days, 8 days, 12 days and 16 days after treatment, respectively. The levels of c-myb and Bcl-2 proteins expression in the three groups were observed by the S-P immunohistochemical method. The results showed the expression of c-myb and bcl-2 proteins was significantly decreased in the AON group, compared with that in the SON and control groups (P < 0.05). These data suggest that c-myb and bcl-2 proteins may play an important role in malignant glioma, and c-myb gene and bcl-2 gene may be involved in the tumorigenesis and development of glioma.
Hua Xi Yi Ke Da Xue Xue Bao 2000 Sep
PMID:[Expression and implication of c-myb and bcl-2 proteins in C6 gliomas]. 1254 15


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