BCL-2 family members and the mitochondria in apoptosis

Gross, Atan; McDonnell, James M.; Korsmeyer, Stanley J.

doi:10.1101/gad.13.15.1899

Cited by 3,376 publications

(2,748 citation statements)

References 119 publications

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“…It is possible that pro-apoptotic molecules other than bax may be more critical in mediating sensitivity to androgen withdrawal in this context. Alternatively, it is conceivable that both an increase in the absolute amount of bax and its appropriate subcellular distribution are necessary to mediate androgen sensitivity (Gross et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

The impact of bcl-2 expression and bax deficiency on prostate homeostasis in vivo

et al. 2000

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Prostatic glandular epithelial cells undergo apoptosis in response to androgen-deprivation. The molecular determinants of androgen-responsiveness in these cells are incompletely understood. Recent evidence suggests that bcl-2 gene family members may be important in this context. We used the probasin promoter to target a human bcl-2 transgene speci®cally to the prostate in order to assess its impact on conferring resistance to androgen withdrawal in, otherwise sensitive, prostatic glandular epithelial cells in vivo. We examined the contribution of bax to mediating androgen-responsiveness in prostatic glandular epithelial cells using bax knockout mice. The histologic appearance of the prostates from probasin-bcl-2 transgenic mice or bax 7/7 mice did not di er from those of control littermates. There was no evidence of hyperplastic or neoplastic growth. There was no di erence between probasin bcl-2 transgenic mice, bax 7/7 mice, and control littermates in steady-state levels of apoptosis. Following castration our ®ndings suggest that both bax and bcl-2 may each contribute to the androgen-responsiveness of prostatic glandular epithelial cells. It is apparent from these results, however, that bax is not required to mediate cell death in prostatic glandular epithelial cells following castration. A comparison between the apoptotic indices in the ventral prostate from the probasin-bcl-2 and bax 7/7 mice following castration suggests that the presence of bcl-2 may be a more important indicator of androgensensitivity than a de®ciency of bax.

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Section: Discussionmentioning

confidence: 99%

The impact of bcl-2 expression and bax deficiency on prostate homeostasis in vivo

et al. 2000

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“…Bax, one of the proteins of the Bcl-2 family is proapoptotic protein and promote apoptosis of cells (Wyllie et al ., 1980; Deckwerth et al ., 1996). Bax activity appears to involve subcellular translocation and dimerization (Gross et al ., 1999). Overexpression of Bax induces the release of cytochrome c, which activates Apaf-1, which is associated caspase-independent activity (Epand et al ., 2002).…”

Section: Disscusionmentioning

confidence: 99%

Neuroprotective Effect of Steamed and Fermented Codonopsis lanceolata

Weon

Yun

Lee

et al. 2014

Biomolecules & Therapeutics

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Codonopsis lanceolata has been used as an herbal medicine for several lung inflammatory diseases, such as asthma, tonsillitis, and pharyngitis. Previously, we showed the neuroprotective effect of steamed and fermented C. lanceolata (SFC) in vitro and in vivo. In the current study, the treatment of HT22 cells with SFC decreased glutamate-induced cell death, suggesting that SFC protected HT22 cells from glutamate-induced cytotoxicity. Based on these, we sought to elucidate the mechanisms of the neuro-protective effect of SFC by measuring the oxidative stress parameters and the expression of Bax and caspase-3 in HT22 cells. SFC reduced contents of ROS, Ca2+ and NO. Moreover, SFC restored contents of glutathione and glutathione reductase as well as inhibited Bax and caspase-3 activity in HT22 cells. These results indicate that steamed and fermented C. lanceolata (SFC) extract protected HT22 cells by anti-oxidative effect and inhibition of the expression of Bax and caspase-3.

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“…These processes are, in part, regulated by members of the Bcl-2 family of cell death factors, some of which are protective and others causative (Green and Reed, 1998;Thornberry and Lazebnik, 1998). The ratio between pro-apoptotic and anti-apoptotic Bcl-2 factors has been shown to modulate the sensitivity of cells to mitochondrial disintegration in response to apoptotic signals (Oltvai et al, 1993;Gross et al, 1999). To elucidate the coordination of myocyte cell cycle withdrawal and apoptosis, we analyzed apoptosisrelated genes during C2C12 differentiation (Table 2).…”

Section: Coordinate Regulation Of Cell Cycle Withdrawal and Apoptosismentioning

confidence: 99%

Genome‐wide examination of myoblast cell cycle withdrawal during differentiation

Shen

Collier

Hlaing

et al. 2002

Developmental Dynamics

105

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Skeletal and cardiac myocytes cease division within weeks of birth. Although skeletal muscle retains limited capacity for regeneration through recruitment of satellite cells, resident populations of adult myocardial stem cells have not been identified. Because cell cycle withdrawal accompanies myocyte differentiation, we hypothesized that C2C12 cells, a mouse myoblast cell line previously used to characterize myocyte differentiation, also would provide a model for studying cell cycle withdrawal during differentiation. C2C12 cells were differentiated in culture medium containing horse serum and harvested at various time points to characterize the expression profiles of known cell cycle and myogenic regulatory factors by immunoblot analysis. BrdU incorporation decreased dramatically in confluent cultures 48 hr after addition of horse serum, as cells started to form myotubes. This finding was preceded by up-regulation of MyoD, followed by myogenin, and activation of Bcl-2. Cyclin D1 was expressed in proliferating cultures and became undetectable in cultures containing 40% fused myotubes, as levels of p21 WAF1/Cip1 increased and ␣-actin became detectable. Because C2C12 myoblasts withdraw from the cell cycle during myocyte differentiation following a course that recapitulates this process in vivo, we performed a genome-wide screen to identify other gene products involved in this process. Using microarrays containing ϳ10,000 minimally redundant mouse sequences that map to the UniGene database of the National Center for Biotechnology Information, we compared gene expression profiles between proliferating, differentiating, and differentiated C2C12 cells and verified candidate genes demonstrating differential expression by RT-PCR. Cluster analysis of differentially expressed genes revealed groups of gene products involved in cell cycle withdrawal, muscle differentiation, and apoptosis. In addition, we identified several genes, including DDAH2 and Ly-6A, whose expression specifically was up-regulated during cell cycle withdrawal coincident with early myoblast differentiation. Developmental Dynamics 226:128 -138, 2003.

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BCL-2 family members and the mitochondria in apoptosis

Cited by 3,376 publications

References 119 publications

The impact of bcl-2 expression and bax deficiency on prostate homeostasis in vivo

The impact of bcl-2 expression and bax deficiency on prostate homeostasis in vivo

Neuroprotective Effect of Steamed and Fermented Codonopsis lanceolata

Genome‐wide examination of myoblast cell cycle withdrawal during differentiation

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