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These results suggest that up-regulation of MVP (show MVP ELISA Kits) in multi-drug resistance (MDR) may involve chromatin remodeling.
Data show that secretion of IL-6 (show IL6 ELISA Kits) induced by loss of HIC1 activated STAT3 (show STAT3 ELISA Kits) through IL-6 (show IL6 ELISA Kits)/JAK (show JAK3 ELISA Kits) pathway and was associated with NSCLC progression.
The VNTR sequence near HIC1 could be a predictive marker for oxaliplatin-based chemotherapy in patients with metastatic colorectal cancer.
Therefore, our data identify HIC1 as a novel factor involved in B cell differentiation acting as an epigenetic repressor of CIITA (show CIITA ELISA Kits) transcription.
HIC1 loss promotes prostate cancer metastasis by triggering epithelial-mesenchymal transition.
Data show that expression of hypermethylated in cancer 1 protein (HIC1) is downregulated in uveal melanoma.
HIC1 attenuates invasion and metastasis by inhibiting the IL-6 (show IL6 ELISA Kits)/STAT3 (show STAT3 ELISA Kits) signalling pathway in human pancreatic ductal adenocarcinoma.
Epigenetic silencing of HIC1 promotes epithelial-mesenchymal transition and drives progression in esophageal squamous cell carcinoma via EphA2 (show EPHA2 ELISA Kits) signaling.
The tumor-suppressive function of Hic1 in colon is related to its inhibitory action on proproliferative signaling mediated by the Tlr2 (show TLR2 ELISA Kits) 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 ELISA Kits) as well as number of cell cycle-related genes, which may or may not be directly linked to p53 (show TP53 ELISA Kits).
We found that EVI1 (show MECOM ELISA Kits) and HIC1 colocalize in the nucleus, and their interaction is mediated by the amino terminal zinc finger binding domain of EVI1 (show MECOM ELISA Kits)
identify HIC1 as the first transcription factor in mammals able to recruit PRC2 to some target promoters through its interaction with Polycomb (show CBX2 ELISA Kits)-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 ELISA Kits) and Sox9 (show SOX9 ELISA Kits).
A potential tumor suppressor role for Hic1 in breast cancer through transcriptional repression of ephrin-A1 (show EFNA1 ELISA Kits).
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 ELISA Kits) mutation
Inactivation of HIC1 results in upregulated SIRT1 (show SIRT1 ELISA Kits) expression in normal or cancer cells; this deacetylates and inactivates p53 (show TP53 ELISA Kits), allowing cells to bypass apoptosis and survive DNA damage.
For the Hic-1 gene, but not p16, the p53 (show TP53 ELISA Kits) gene might protect against aberrant methylation. The iNOS (show NOS2 ELISA Kits) 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 ELISA Kits) 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