HSF4 Antibody (N-term) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Primary Accession | Q9ULV5 |
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Clone Names | 100528196 |
Gene ID | 3299 |
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Other Names | Heat shock factor protein 4, HSF 4, hHSF4, Heat shock transcription factor 4, HSTF 4, HSF4 |
Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
Name | HSF4 |
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Function | Heat-shock transcription factor that specifically binds heat shock promoter elements (HSE) (PubMed:22587838, PubMed:23507146). Required for denucleation and organelle rupture and degradation that occur during eye lens terminal differentiation, when fiber cells that compose the lens degrade all membrane-bound organelles in order to provide lens with transparency to allow the passage of light (By similarity). In this process, may regulate denucleation of lens fiber cells in part by activating DNASE2B transcription (By similarity). May be involved in DNA repair through the transcriptional regulation of RAD51 (PubMed:22587838). May up-regulate p53/TP53 protein in eye lens fiber cells, possibly through protein stabilization (PubMed:28981088). In the eye lens, controls the expression of alpha-crystallin B chain/CRYAB and consequently may be involved in the regulation of lysosomal acidification (By similarity). |
Cellular Location | Nucleus. |
Tissue Location | Expressed in heart, skeletal muscle, eye and brain, and at much lower levels in some other tissues |
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Provided below are standard protocols that you may find useful for product applications.
Background
Heat-shock transcription factors (HSFs) activateheat-shock response genes under conditions of heat or otherstresses. HSF4 lacks the carboxyl-terminal hydrophobic repeat whichis shared among all vertebrate HSFs and has been suggested to beinvolved in the negative regulation of DNA binding activity. Twoalternatively spliced transcripts encoding distinct isoforms andpossessing different transcriptional activity have been described.
References
Bailey, S.D., et al. Diabetes Care 33(10):2250-2253(2010)Enoki, Y., et al. Biochim. Biophys. Acta 1802(9):749-753(2010)Ma, Z.Y., et al. Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 26(4):325-328(2010)Talmud, P.J., et al. Am. J. Hum. Genet. 85(5):628-642(2009)Sajjad, N., et al. BMC Med. Genet. 9, 99 (2008) :
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