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KDM5C is a member of the SMCY homolog family and encodes a protein with one ARID domain, one JmjC domain, one JmjN domain and two PHD-type zinc fingers. Additionally we are shipping KDM5C Antibodies (53) and KDM5C Proteins (4) and many more products for this protein.
KDM5C expression was generally lower in cancer lesions compared with matched nontumor tissues. KDM5C has a vital function in inhibiting cell mobility, which is at least partially controlled by the p53 (show TP53 ELISA Kits).
Mutation in KDM5C gene is associated with cancer more frequently in males.
In vitro models indicated that KDM5C suppressed miR (show MLXIP ELISA Kits)-320a transcription by directly binding to the promoter of miR (show MLXIP ELISA Kits)-320a to prevent histone methylation. KITLG (show KITLG ELISA Kits), an essential gene for ovarian development and primordial germ cell survival, was a direct target of miR (show MLXIP ELISA Kits)-320a and that it was downregulated in 45,X fetal gonadal tissues.
The two mutations are present on the same maternal haplotype, suggesting that a postzygotic somatic mutation or a reversion error occurred at an early embryonic stage in the mother, leading to switched KDM5C mutations in the affected siblings.
The predicted structure of KDM5C was used to investigate the effects of disease-causing mutations, and it was shown that the mutations alter domain stability and inter-domain interactions.
Results suggest that KDM5C mutations predispose to X-linked intellectual disability which accounts for 1-4% of cases in male patient.
the extent of the duplicated regions in each case encompassing a minimum of three known disease genes TSPYL2 (show TSPYL2 ELISA Kits), KDM5C and IQSEC2 (show IQSEC2 ELISA Kits), is reported.
KDM5C is overexpressed in breast cancer cells and miR (show MLXIP ELISA Kits)-138 regulates its expression.
study of non-synonymous mutations in the KDM5C ARID domain and evaluates effects of 2 syndromic Claes-Jensen-type disease-associated missense mutations (A77T and D87G) and 3 non-classified missense mutations (R108W, N142S, and R179H); analysis indicates, among the non-classified mutations, R108W is possibly a disease-associated mutation, and N142S and R179H are probably harmless
Findings reveal a RACK7/KDM5C-regulated, dynamic interchange between histone H3K4me1 and H3K4me3 at active enhancers, representing an additional layer of regulation of enhancer activity. Authors propose that RACK7/KDM5C functions as an enhancer "brake" to ensure appropriate enhancer activity, which, when compromised, could contribute to tumorigenesis.
The results identify two key regulators, PCGF6 (show PCGF6 ELISA Kits) and JARID1c that temper dendritic cells (DC) activation and implicate active transcriptional silencing via histone demethylation as a previously unappreciated mechanism for regulating DC activation and quiescence.
Neurite growth in Neuro2a cells was suppressed by the KDM5C mutations associated with intellectual disability in patients. Ntng2 was downregulated in cells with KDM5C mutations, concordant with the lower levels of H3K4 methylation at its promoter.
these data suggest that inactivation of JARID1C in renal cancer leads to heterochromatin disruption, genomic rearrangement, and aggressive ccRCCs.
The present study was designed to detect the expression of Histone H3 (show HIST3H3 ELISA Kits) lysine 4 methylation and its demethylases LSD1 (show KDM1A ELISA Kits), RBP2 (show RBP2 ELISA Kits) and SMCX in 21-, 40- and 60-day-old mouse testes.
Kdm5c protein restricts transcriptional output at promoters, whereas Kdm5c binding to enhancers stimulates their activity.
sex-specific expression of Jarid1c may contribute to sex differences in brain function
allelic expression and RNA/DNA FISH indicate that transgenic Jarid1c escapes X inactivation.
The full-length cDNA of JARID1C has been cloned.
This gene is a member of the SMCY homolog family and encodes a protein with one ARID domain, one JmjC domain, one JmjN domain and two PHD-type zinc fingers. The DNA-binding motifs suggest this protein is involved in the regulation of transcription and chromatin remodeling. Mutations in this gene have been associated with X-linked mental retardation. Alternative splicing results in multiple transcript variants.
histone demethylase JARID1C
, lysine (K)-specific demethylase 5C
, jumonji, AT rich interactive domain 1C
, JmjC domain-containing protein SMCX
, Jumonji, AT rich interactive domain 1C (RBP2-like)
, Jumonji/ARID domain-containing protein 1C
, Smcx homolog, X chromosome
, Smcy homolog, X-linked
, lysine-specific demethylase 5C
, protein SmcX
, selected cDNA on X
, jumonji, AT rich interactive domain 1C (Rbp2 like)
, jumonji/ARID domain-containing protein 1C
, selected mouse cDNA on the X
, lysine (K)-specific demethylase 5C tv1
, Lysine-specific demethylase 5C