ArticleThe Journal of biological chemistry2010
FKBP38 protects Bcl-2 from caspase-dependent degradation.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 42 citations in OpenAlex.
- The sulfonamide anticancer agent indisulam enhances the chemosensitivity of gastric cancer cells by targeting FKBP8.The FEBS journal · 2026Article
- Dysferlin Protein-Protein Interaction Pathways in the Organ of Corti and Spiral Ganglion Intersect with Alzheimer's Protein Pathways.International journal of molecular sciences · 2025Article
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- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022Article
- FBXO7 triggers caspase 8-mediated proteolysis of the transcription factor FOXO4 and exacerbates neuronal cytotoxicity.The Journal of biological chemistry · 2021Article
- Prohibitin regulates mTOR pathway via interaction with FKBP8.Frontiers of medicine · 2021Article
- FKBP8 protects the heart from hemodynamic stress by preventing the accumulation of misfolded proteins and endoplasmic reticulum-associated apoptosis in mice.Journal of molecular and cellular cardiology · 2018Article
- FKBP8 recruits LC3A to mediate Parkin-independent mitophagy.EMBO reports · 2017Article
- Association of single nucleotide polymorphisms in the coding region of Bcl-2 with the occurrence and prognosis of colorectal cancer: A case-control study.Cancer biomarkers : section A of Disease markers · 2017Article
- FK506-Binding Proteins and Their Diverse Functions.Current molecular pharmacology · 2015Review
- Crystal structure and conformational flexibility of the unligated FK506-binding protein FKBP12.6.Acta crystallographica. Section D, Biological crystallography · 2014Article
- Adamantyl derivative as a potent inhibitor of Plasmodium FK506 binding protein 35.ACS medicinal chemistry letters · 2013Article
- RRM2 regulates Bcl-2 in head and neck and lung cancers: a potential target for cancer therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Article
- Small molecule Plasmodium FKBP35 inhibitor as a potential antimalaria agent.Scientific reports · 2013Article
- High-resolution crystal structure of FKBP12 from Aedes aegypti.Protein science : a publication of the Protein Society · 2012Article
- FK506 binding protein 8 peptidylprolyl isomerase activity manages a late stage of cystic fibrosis transmembrane conductance regulator (CFTR) folding and stability.The Journal of biological chemistry · 2012Article
- The FKBP38 catalytic domain binds to Bcl-2 via a charge-sensitive loop.The Journal of biological chemistry · 2012Article
- FKBP38 peptidylprolyl isomerase promotes the folding of cystic fibrosis transmembrane conductance regulator in the endoplasmic reticulum.The Journal of biological chemistry · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cellular processes that regulate Bcl-2 at the posttranslational levels are as important as those that regulate bcl-2 synthesis. Previously we demonstrated that the suppression of FK506-binding protein 38 (FKBP38) contributes to the instability of Bcl-2 or leaves Bcl-2 unprotected from degradation in an unknown mechanism. Here, we studied the underlying molecular mechanism mediating this process. We first showed that Bcl-2 binding-defective mutants of FKBP38 fail to accumulate Bcl-2 protein. We demonstrated that the FKBP38-mediated Bcl-2 stability is specific as the levels of other anti-apoptotic proteins such as Bcl-X(L) and Mcl-1 remained unaffected. FKBP38 enhanced the Bcl-2 stability under the blockade of de novo protein synthesis, indicating it is posttranslational. We showed that the overexpression of FKBP38 attenuates reduction rate of Bcl-2, thus resulting in an increment of the intracellular Bcl-2 level, contributing to the resistance of apoptotic cell death induced by the treatment of kinetin riboside, an anticancer drug. Caspase inhibitors markedly induced the accumulation of Bcl-2. In caspase-3-activated cells, the knockdown of endogenous FKBP38 by small interfering RNA resulted in Bcl-2 down-regulation as well, which was significantly recovered by the treatment with caspase inhibitors or overexpression of FKBP38. Finally we presented that the Bcl-2 cleavage by caspase-3 is blocked when Bcl-2 binds to FKBP38 through the flexible loop. Taken together, these results suggest that FKBP38 is a key player in regulating the function of Bcl-2 by antagonizing caspase-dependent degradation through the direct interaction with the flexible loop domain of Bcl-2, which contains the caspase cleavage site.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.