ArticleJournal of cellular biochemistry2009
Heat shock factor 1 deficiency via its downstream target gene alphaB-crystallin (Hspb5) impairs p53 degradation.
Article in Journal of cellular biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Regulation of human papillomavirus E6 oncoprotein function via a novel ubiquitin ligase FBXO4.mBio · 2025Article
- SKP1-CUL1-F-box: Key molecular targets affecting disease progression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Tumor suppressor p53 regulates heat shock factor 1 protein degradation in Huntington's disease.Cell reports · 2023Article
- Targeted Replacement of HSF1 Phosphorylation Sites at S303/S307 with Alanine Residues in Mice Increases Cell Proliferation and Drug Resistance.Methods in molecular biology (Clifton, N.J.) · 2023Article
- HSF1 and Its Role in Huntington's Disease Pathology.Advances in experimental medicine and biology · 2023Review
- The E3 Ubiquitin Ligase Fbxo4 Functions as a Tumor Suppressor: Its Biological Importance and Therapeutic Perspectives.Cancers · 2022Review
- Cluster analyses of the TCGA and a TMA dataset using the coexpression of HSP27 and CRYAB improves alignment with clinical-pathological parameters of breast cancer and suggests different epichaperome influences for each sHSP.Cell stress & chaperones · 2021Article
- Excitatory synapse impairment and mitochondrial dysfunction in Huntington's disease: heat shock factor 1 (HSF1) converging mechanisms.Neural regeneration research · 2020Article
- Interplay between HSF1 and p53 signaling pathways in cancer initiation and progression: non-oncogene and oncogene addiction.Cellular oncology (Dordrecht, Netherlands) · 2019Review
- High α B-crystallin and p53 co-expression is associated with poor prognosis in ovarian cancer.Bioscience reports · 2019Article
- Mitochondrial Dysfunction in Huntington's Disease; Interplay Between HSF1, p53 and PGC-1α Transcription Factors.Frontiers in cellular neuroscience · 2019Article
- The heat-shock, or HSF1-mediated proteotoxic stress, response in cancer: from proteomic stability to oncogenesis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018Review
- Targeted Deletion of Hsf1, 2, and 4 Genes in Mice.Methods in molecular biology (Clifton, N.J.) · 2018Article
- αB-crystallin: Portrait of a malignant chaperone as a cancer therapeutic target.Pharmacology & therapeutics · 2016Review
- Defective heat shock factor 1 inhibits the growth of fibrosarcoma derived from simian virus 40/T antigen‑transformed MEF cells.Molecular medicine reports · 2015Article
- Upregulation of heat shock factor 1 transcription activity is associated with hepatocellular carcinoma progression.Molecular medicine reports · 2014Article
- Pleiotropic role of HSF1 in neoplastic transformation.Current cancer drug targets · 2014Review
- Chaperones: needed for both the good times and the bad times.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2013Article
- Heat shock factor Hsf1 cooperates with ErbB2 (Her2/Neu) protein to promote mammary tumorigenesis and metastasis.The Journal of biological chemistry · 2012Article
- Inactivation of heat shock factor Hsf4 induces cellular senescence and suppresses tumorigenesis in vivo.Molecular cancer research : MCR · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Heat shock factor Hsf1 regulates the stress-inducibility of heat shock proteins (Hsps) or molecular chaperones. One of the functions attributed to Hsps is their participation in folding and degradation of proteins. We recently showed that hsf1(-/-) cells accumulate ubiquitinated proteins. However, a direct role for Hsf1 in stability of specific proteins such as p53 has not been elucidated. We present evidence that cells deficient in hsf1 accumulate wild-type p53 protein. We further show that hsf1(-/-) cells express lower levels of alphaB-crystallin and cells deficient in alphaB-crystallin also accumulate p53 protein. Reports indicate that alphaB-crystallin binds to Fbx4 ubiquitin ligase, and they target cyclin D1 for degradation through a pathway involving the SCF (Skp1-Cul1-F-box) complex. Towards determining a mechanism for p53 degradation involving alphaB-crystallin and Hsf1, we have found that ectopic expression of Fbx4 in wild-type mouse embryo fibroblasts (MEFs) expressing mutant p53 (p53R175H) leads to increase in its degradation, while MEFs deficient in hsf1 or alphaBcry are defective in degradation of this p53 protein. In addition, immunoprecipitated p53R175H from wild-type MEFs is able to pull-down both alphaB-crystallin and Fbx4. Finally, immunoprecipitated wild-type p53 from doxorubicin treated U2OS cells can pull-down endogenous alphaB-crystallin and Fbx4. These results indicate that hsf1- and alphaBcry-deficient cells accumulate p53 due to reduced levels of alphaB-crystallin in these cells. Elevated levels of p53 in hsf1- and alphaBcry-deficient cells lead to their increased sensitivity to DNA damaging agents. These data reveal a novel mechanism for protein degradation through Hsf1 and alphaB-crystallin.
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Registered trials
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