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Expression of the c-myc gene, which produces an oncogenic transcription factor, is tightly regulated in normal cells but is frequently deregulated in human cancers. Additionally we are shipping MXI1 Antibodies (48) and MXI1 Proteins (7) and many more products for this protein.
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The mesangial cell apoptosis observed in this mesangial proliferative glomerulonephritis model was related to CXCL10 (show CXCL10 ELISA Kits) expression induced by Mxi1 inactivation.
Mxi1 regulates Ift20 (show IFT20 ELISA Kits) promoter activity via Ets-1 (show ETS1 ELISA Kits) binding to the Ift20 (show IFT20 ELISA Kits) promoter. These results indicate that inactivating Mxi1 induces ciliary defects in polycystic kidney.
The results support the suggestion that over-expression of Mxi1 can suppress renal epithelial tubulogenesis.
The results support the suggestion that inactivation of Mxi1 has a positive effect on cell proliferation by down-regulating IGFBP-3 (show IGFBP3 ELISA Kits).
down-regulation of miR (show MLXIP ELISA Kits)-191 is essential for erythroid chromatin condensation and enucleation by allowing up-regulation of Riok3 (show RIOK3 ELISA Kits) and Mxi1
Mxi1-SRalpha (show SRPR ELISA Kits) is an isoform with enhanced transcriptional repression potential
Apolipoprotein A1 (show APOA1 ELISA Kits) which is a major component of the high-density lipoprotein complex and has anti-inflammation effects, was significantly decreased in the Mxi1-deficient mouse.
MYC (show MYC ELISA Kits)-HEG and MXI1-LEG levels are associated with poor prognosis in patients with breast cancer, suggesting that they may be useful molecular markers in breast cancer prognosis prediction.
MicroRNA-155 promotes glioma cell proliferation via the regulation of MXI1.
MXI1-0 appears to be a downstream target of MYCN (show MYCN ELISA Kits)-dependent signaling pathways and may contribute to N-Myc (show MYCN ELISA Kits)-dependent cell growth and proliferation.
These findings reveal, for the first time, the novel functions of cooperation of miR243p and miR27a3p from two clusters in promoting cell proliferation through MXI1.
Mxi1 can act as a tumour suppressor in human glioblastomas through a molecular mechanism involving the transcriptional down-regulation of cyclin B1 (show CCNB1 ELISA Kits) gene expression.
These findings support MXI1 as a putative tumor suppressor gene involved in conventional melanoma progression.
Data show that PTEN and MXI1 were two candidate tumor suppressor genes on 10q23 and 10q24-q25 and may be potentially involved in the initiation and progression of prostate carcinoma.
Mxi-D may play an important role in the c-Myc (show MYC ELISA Kits) family protein network acting as a dominant negative isoform of Mxi-F stimulated by c-Myc (show MYC ELISA Kits)
p300 (show EP300 ELISA Kits) can acetylate DNA-bound Myc:Max complexes and that acetylated Myc:Max heterodimers efficiently interact with Miz-1 (show ZBTB17 ELISA Kits)
Expression of the c-myc gene, which produces an oncogenic transcription factor, is tightly regulated in normal cells but is frequently deregulated in human cancers. The protein encoded by this gene is a transcriptional repressor thought to negatively regulate MYC function, and is therefore a potential tumor suppressor. This protein inhibits the transcriptional activity of MYC by competing for MAX, another basic helix-loop-helix protein that binds to MYC and is required for its function. Defects in this gene are frequently found in patients with prostate tumors. Three alternatively spliced transcripts encoding different isoforms have been described. Additional alternatively spliced transcripts may exist but the products of these transcripts have not been verified experimentally.
max interactor 1
, MAX interactor 1
, adducin 3 (gamma)
, max-interacting protein 1
, MAX interacting protein 1
, Max interacting protein 1
, MAX dimerization protein 2
, Max-related transcription factor
, class C basic helix-loop-helix protein 11