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HIC1 functions as a growth regulatory and tumor repressor gene. Additionally we are shipping HIC1 Antibodies (75) and HIC1 Kits (3) and many more products for this protein.
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These results suggest that up-regulation of MVP (show MVP Proteins) in multi-drug resistance (MDR) may involve chromatin remodeling.
Epigenetic silencing of HIC1 promotes epithelial-mesenchymal transition and drives progression in esophageal squamous cell carcinoma via EphA2 (show EPHA2 Proteins) signaling.
The tumor-suppressive function of Hic1 in colon is related to its inhibitory action on proproliferative signaling mediated by the Tlr2 receptor present on tumor cells.
Results demonstrated an important role of HIC1 for the normal progression of cell cycle, and could affect the homeostasis of p53 (show TP53 Proteins) as well as number of cell cycle-related genes, which may or may not be directly linked to p53 (show TP53 Proteins).
We found that EVI1 (show MECOM Proteins) and HIC1 colocalize in the nucleus, and their interaction is mediated by the amino terminal zinc finger binding domain of EVI1 (show MECOM Proteins)
HIC-1 expression was assessed on a tissue microarray containing 80 cases of breast cancer.
Hypermethylation of HIC1 promoter and aberrant expression of HIC1/SIRT1 (show SIRT1 Proteins) might contribute to the carcinogenesis of pancreatic cancer.
ectopic expression of HIC1 in U2OS and MDA-MB-231 cell lines decreases expression of the ApoER2 (show LRP8 Proteins) and VLDLR (show VLDLR Proteins) genes, encoding two canonical tyrosine kinase (show TXK Proteins) receptors for Reelin (show RELN Proteins).
HIC1 silencing in triple-negative breast cancer drives progression through misregulation of LCN2 (show LCN2 Proteins).
HIC1 interacts with and modulates the transcriptional activity of STAT3 (show STAT3 Proteins).
Reactivation of HIC1 suppressed cell migration and induced cell cycle arrest in the G0/G1 phase, as well as induced apoptosis in gastric cancer cells.
identify HIC1 as the first transcription factor in mammals able to recruit PRC2 to some target promoters through its interaction with Polycomb (show CBX2 Proteins)-like proteins.
Data show that Hic1 expression is absent in polyps from DH mice, with concomitant increased expression of two transcriptional repression targets of Hic1, Sirt1 (show SIRT1 Proteins) and Sox9 (show SOX9 Proteins).
A potential tumor suppressor role for Hic1 in breast cancer through transcriptional repression of ephrin-A1 (show EFNA1 Proteins).
mice disrupted in the germ line for only one allele of Hic1 develop many different spontaneous malignant tumors, including a predominance of epithelial cancers in males and lymphomas and sarcomas in females
In human osteosarcomas, hypermethylation of HIC1 is frequent only in tumors with p53 (show TP53 Proteins) mutation
Inactivation of HIC1 results in upregulated SIRT1 (show SIRT1 Proteins) expression in normal or cancer cells; this deacetylates and inactivates p53 (show TP53 Proteins), allowing cells to bypass apoptosis and survive DNA damage.
For the Hic-1 gene, but not p16, the p53 (show TP53 Proteins) gene might protect against aberrant methylation. The iNOS (show NOS2 Proteins) gene might not be involved in methylation of the Hic-1 gene, whereas the promoter region of p16 could be prone to methylation in MEFs lacking the iNOS (show NOS2 Proteins) gene.
This gene functions as a growth regulatory and tumor repressor gene. Hypermethylation or deletion of the region of this gene have been associated with tumors and the contiguous-gene syndrome, Miller-Dieker syndrome. Alternative splicing of this gene results in multiple transcript variants.
, hypermethylated in cancer 1 protein
, hypermethylated in cancer 1
, zinc finger and BTB domain-containing protein 29
, hypermethylated in cancer 1 protein-like