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We have identified a novel mutation in HSF4 in a large British pedigree causing dominant congenital lamellar cataract
High HSF4 expression is an independent indicator of poor overall survival and recurrence free survival in patients with primary colorectal cancer.
In the cultured human lens epithelial cells, HSF4 could stabilize and retain p53 in the nucleus to activate its target genes such as fas cell surface death receptor (Fas) and Bcl-2-associated X apoptosis regulator (Bax).
HMOX-1, an anti-oxidase, is a bona fide transcriptional target gene of HSF4 in HLECs (human lens epithelial cells). HSF4 directly binds to the HSE element in HMOX-1 promoter to mediate its mRNA transcription and protein accumulation.
report on a novel homozygous HSF4 mutation (c.521T>C, p.Leu174Pro) in two sibs with congenital cataracts
BCAS2 interacts with HSF4 and negatively regulates its protein stability via ubiquitination.
HSF4 may work as a switch between lens epithelial cell proliferation and secondary fiber cell differentiation, a process which mainly depends on p53.
Nuclear HSF2 and HSF4 bound to HSF1 only after heat shock.
concluded that the new mutation of c.331C>T in HSF4 DNA may be responsible for the autosomal dominant congenital cataract in this family
We found that HSF4 downregulation led to decrease of HIF1alpha mRNA expression
HSF4 p.Arg116His recreates the childhood lamellar cataract in mice suggesting that incomplete penetrance associated with early cataracts may not be an absence but a limitation of the detection of the phenotype
This is the first report of the novel missense mutation, c.69 G-->T (p. K23N), in exon 3 of the HSF4 locus on 16q21-q22 associated with bilateral congenital cataracts in a Chinese family.
the transcriptional activation of HSF4 is mediated by interactions between activator and repressor domains within the C-terminal end.
This comparative analysis with CRYAB and HSP70 demonstrates that differential heat shock response is controlled by cell-type-dependent access of HSF1 and HSF4 to specific promoters, independent of the promoter architecture.
HSF4 exerts its function on lens differentiation via positive regulation of DLAD expression.
HSF4 and WRN CNVs might be involved in ARC pathogenesis in the Han Chinese.
Presents the first evidence demonstrating that HSF4 plays a role in DNA damage repair and may contribute a better understanding of congenital cataract formation.
we report the absence of mutations in all studied genes in four families with phenotypes associating cataract, mental retardation and microcephaly.
our findings suggest novel mechanisms of HSF2 regulation controlled by HSF4a.
HSF2 and HSF4 regulate transcription of HIF-1a and that a critical balance between these HSF is required to maintain HIF-a expression in a repressed state.
a novel molecular mechanism of HSF4 in regulating lens epithelial cell homeostasis
The deletion of Hsf4 affects the expression of many genes, such as Ubc, Ptgs2, Egr1 and Fos. These genes may be involved in the development of cataract.
A novel regulatory mechanism between Hsf1 and Hsf4b in modulating lens epithelial cell homeostasis.
Mutations in the DNA binding domain (DBD) of the heat shock transcription factor 4 (HSF4) are known to be associated with early childhood autosomal dominant lamellar cataract.
Hsf4b is a novel downstream transcription factor of FGF2, and its transcription activity is associated with FGF2-modulated lens epithelial cell-fiber cell transition.
Mutation in HSF4b abolishes its function. Loss of 132 amino acids from the COOH-terminus of a mouse cataract HSF4b(lop11) results in the failure of trimer formation and subsequent failure of target DNA binding and transactivation.
These results revealed an essential role for HSF4-mediated SKAP2 expression in the regulation of actin reorganization during lens differentiation.
Data reveal the lens-specific role of heat shock transcription factor 4 (HSF4), and indicate that HSF1 and HSF4 are involved in regulating expression of growth factor genes.
HSF4 fulfills a central role in controlling spatial and temporal expression of genes critical for correct development and function of the lens.
Molecular evaluation of Hsf4 revealed an early transposable element inserted in intron 9 leading to cataract formation.
analysis of mechanisms of gene regulation controlled by HSF4 in non-classic heat shock response and in lens development
disruption of the Hsf4 gene leads to cataracts via at least three pathways: down-regulation of gamma-crystallin, particularly gamma S-crystallin; decreased lens beaded filament expression; and loss of post-translational modification of alpha A-crystallin
In the hsf4(null) fish, both p53 and activated-caspase3 were significantly decreased. Combined with the finding that the denucleation defect could be partially rescued through microinjection of p53, fas and bax mRNA into the mutant embryos, we directly proved that HSF4 promotes lens fiber cell differentiation by activating p53 and its downstream regulators
Heat-shock transcription factors (HSFs) activate heat-shock response genes under conditions of heat or other stresses. HSF4 lacks the carboxyl-terminal hydrophobic repeat which is shared among all vertebrate HSFs and has been suggested to be involved in the negative regulation of DNA binding activity. Two alternatively spliced transcripts encoding distinct isoforms and possessing different transcriptional activity have been described.
, HSTF 4
, heat shock factor protein 4
, DNA binding protein
, binds heat shock DNA elements
, heat shock factor 4
, heat shock transcription factor 4 variant a
, heat shock transcription factor 4 variant b
, heat shock transcription factor 4 variant c