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

BAG-1 protein was initially identified as a Bcl-2-binding protein. It was reported to enhance Bcl-2 protection from cell death, suggesting that BAG-1 represents a new type of anti-cell death gene. Moreover, recent study has shown that BAG-1 can enhance the proliferation of neuronal precursor cells, attenuate the growth inhibition induced by siah1. However, its function and expression in the central nervous system lesion are not been understood very well. In this study, we performed a traumatic brain injury (TBI) model in adult rats and investigated the dynamic changes of BAG-1 expression in the brain cortex. Double immunofluorescence staining revealed that BAG-1 was co-expressed with NEURON and glial fibrillary acidic protein (GFAP). In addition, we detected that proliferating cell nuclear antigen had the co-localization with GFAP, and BAG-1. All our findings suggested that BAG-1 might involve in the pathophysiology of brain after TBI.
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PMID:Increased expression of BAG-1 in rat brain cortex after traumatic brain injury. 2252 8

Experimentally induced androgen deficiency during late pregnancy leads to decreased progesterone synthesis in the porcine corpus luteum (CL), which suggested an onset of functional luteolysis. It was shown that luteal regression in mammals involves not only apoptosis but also autophagy. Therefore, this study aimed to examine whether anti-androgen flutamide treatment during late pregnancy in pigs induces apoptosis and/or autophagy within luteal cells. Flutamide (50 mg/kg b.w.) was administered into pregnant gilts between 83 - 89 (GD90F) or 101 - 107 (GD108F) gestational days (GD). CLs were retrieved on day 90 or 108 of pregnancy (n = 3/each group). Detection of apoptosis was performed by TUNEL assay and assessment of cleaved caspase 3 level. Both assays revealed that luteal rate of apoptosis was unaffected by flutamide treatment either in the GD90F or GD108F groups. Moreover, pro-apoptotic protein Bax was downregulated on GD108. The autophagy was examined by expression of two markers, LC3-II and Lamp1. Flutamide led to greater expression of LC3-II protein form in the GD90F and GD108F groups. Likewise, the mRNA and protein levels of Lamp1 were elevated in both flutamide-treated groups. The activation of autophagy is regulated by Beclin 1 and the increased Beclin 1 mRNA and protein expression was found in the GD90F and GD108F groups. Beclin 1 is a Bcl-2-binding protein, thus Beclin1/Bcl-2 interactions were examined using immunoprecipitation. Beclin 1/Bcl-2 complexes were less abundant following flutamide treatment in both flutamide-exposed groups. In summary, we concluded that androgen deficiency induced autophagy by disrupting Beclin 1/Bcl-2 interplay in the porcine CL during pregnancy. The role of autophagy in luteal regression in pigs requires further evaluation.
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PMID:Induction of autophagy in the porcine corpus luteum of pregnancy following anti-androgen treatment. 2819 74


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