Disease relevance of Bcl2l2

• We detected higher levels of Bcl-w in hippocampus from temporal lobe epilepsy patients compared with autopsy controls [1].

High impact information on Bcl2l2

• Epidermal growth factor receptor stimulation resulted in a decreased ratio of Bax to Bcl-w expression and decreased rates of apoptosis [2].
• CONCLUSIONS: The crypt expression of Bax and Bcl-w is influenced by epidermal growth factor receptor signaling and is key for the regulation of apoptosis [2].
• Bcl-w-null mice had poor survival and impaired adaptation to small-bowel resection, an effect that was rescued by crossbreeding these mice with epidermal growth factor transgenic mice [2].
• Apoptosis regulator bcl-w is essential for spermatogenesis but appears otherwise redundant [3].
• We used microinjection to introduce expression plasmids containing Bcl-w and Bcl-x(L) cDNAs in the sense and antisense orientations into the nuclei of BDNF-dependent nodose neurons and NGF-dependent trigeminal neurons at stages during and after the period of naturally occurring neuronal death [4].

Biological context of Bcl2l2

• Comparison of the expected amino acid sequence of Bcl-w with that of these relatives helps to delineate residues likely to convey survival or anti-survival function [5].
• As Bclw is expressed in both Sertoli cells and diploid male germ cells, it has been unclear which of these cell types requires BCLW in a cell-autonomous manner for survival [6].
• In situ hybridization analysis indicates that Bclw is expressed in Sertoli cells both before and after exit from mitosis [6].
• Thus, Bak and Bcl-w may regulate cell death through independent pathways [7].
• To determine if changes in Bak and Bcl-w expression could regulate mammary apoptosis, their effect on cultured mouse mammary epithelial cells was examined in transient transfection assays [7].

Anatomical context of Bcl2l2

• Therefore, Bclw-independent pathways promote the survival of undifferentiated, mitotic Sertoli cells [6].
• RESULTS: When compared with Bcl-w, the most significant expression changes were observed with Bax and took place within crypt enterocytes [2].
• Reciprocal developmental changes in the roles of Bcl-w and Bcl-x(L) in regulating sensory neuron survival [4].
• There was a marked increased in Bcl-w mRNA and Bcl-w immunoreactive neurons and a decrease in Bcl-x(L) mRNA and Bcl-x(L) immunoreactive neurons in the trigeminal and nodose ganglia over this period of development [4].
• In the adult rat testis, both Bcl-w mRNA and protein in Sertoli cells displayed a stage-specific expression pattern [8].

Associations of Bcl2l2 with chemical compounds

• FSH could up-regulate Bcl-w mRNA levels in the seminiferous tubules cultured in vitro, whereas no effect was observed when testosterone was applied [8].
• Serine phosphorylation of Bcl-xL and Bcl-w correlates with the number of trimolecular complexes formed [9].
• The increases of mRNA levels of Bcl-2 and Bcl-w were observed for the first 3 h of C2-ceramide treatment and the last 24 h between 24 and 48 h [10].
• Fas, Fas-L and Bcl-w expression were analyzed semiquantitatively by RT-PCR immediately after potassium iodide administration (group MI44D) or at week 32 (MI32S) [11].
• Effect of iodide on Fas, Fas-ligand and Bcl-w mRNA expression in thyroid of NOD mice pretreated with methimazole [11].

Physical interactions of Bcl2l2

• Bcl-xL and Bcl-w specifically interact with PP1alpha and Bad [9].

Regulatory relationships of Bcl2l2

• While mutation of Bak had no effect, ablation of Bax suppressed the loss of Sertoli cells in Bclw mutants [6].

Other interactions of Bcl2l2

• To determine whether death of Sertoli cells in Bclw mutants is influenced by the protracted loss of germ cells, we examined testes from Bclw/c-kit double mutant mice, which lack germ cells from birth [6].
• Survival activity of Bcl-2 homologs Bcl-w and A1 only partially correlates with their ability to bind pro-apoptotic family members [12].
• Bax and Bak were immunohistochemically localized to the same cell types as Bcl-w, but with higher expression levels in spermatocytes and spermatogonia than in Sertoli cells [8].
• In contrast, a significant increase was observed in the anti-apoptotic member Bcl-2. mRNA expression of Bcl-w, Bad, and Bcl-x(L) was not significantly different between the control and TPN groups [13].
• Epidermal growth factor receptor signaling regulates Bax and Bcl-w expression and apoptotic responses during intestinal adaptation in mice [2].

Analytical, diagnostic and therapeutic context of Bcl2l2

• Mitochondria appeared to be swollen and the cytoplasm dense by electron microscopy, but degenerating Bclw-deficient Sertoli cells failed to display classical features of apoptosis, such as chromatin condensation and nuclear fragmentation [14].
• Immunoblotting data revealed similar increases of c98 protein expression to its mRNA expression in the keratinocytes of IGF-1-injected animals [15].
• Subcellular fractionation and confocal laser scanning microscopy demonstrated that Bcl-w protein is associated with intracellular membranes [16].
• Gene targeting experiments in mice have demonstrated that Bcl-w is required for spermatogenesis and for survival of damaged epithelial cells in the gut [16].

References