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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. Zusätzlich bieten wir Ihnen MAX Interactor 1 Proteine (10) und MAX Interactor 1 Kits (3) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 50 products:
Human Polyclonal MXI1 Primary Antibody für EIA,WB - ABIN953554
Löfstedt, Fredlund, Noguera, Navarro, Holmquist-Mengelbier, Beckman, Påhlman, Axelson: HIF-1alpha induces MXI1 by alternate promoter usage in human neuroblastoma cells. in Experimental cell research 2009
Zeige alle 3 Referenzen für ABIN953554
Chicken Polyclonal MXI1 Primary Antibody für IHC,WB - ABIN971213
Dugast-Darzacq, Pirity, Blanck, Scherl, Schreiber-Agus: Mxi1-SRalpha: a novel Mxi1 isoform with enhanced transcriptional repression potential. in Oncogene 2004
Chicken Polyclonal MXI1 Primary Antibody für WB - ABIN404744
Dugast-Darzacq, Grange, Schreiber-Agus: Differential effects of Mxi1-SRalpha and Mxi1-SRbeta in Myc antagonism. in The FEBS journal 2007
The mesangial cell apoptosis observed in this mesangial proliferative glomerulonephritis model was related to CXCL10 (zeige CXCL10 Antikörper) expression induced by Mxi1 inactivation.
Mxi1 regulates Ift20 (zeige IFT20 Antikörper) promoter activity via Ets-1 (zeige ETS1 Antikörper) binding to the Ift20 (zeige IFT20 Antikörper) 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 (zeige IGFBP3 Antikörper).
down-regulation of miR (zeige MLXIP Antikörper)-191 is essential for erythroid chromatin condensation and enucleation by allowing up-regulation of Riok3 (zeige RIOK3 Antikörper) and Mxi1
Mxi1-SRalpha (zeige SRPR Antikörper) is an isoform with enhanced transcriptional repression potential
Apolipoprotein A1 (zeige APOA1 Antikörper) 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 (zeige MYC Antikörper)-HEG (zeige HEG1 Antikörper) 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 (zeige MYCN Antikörper)-dependent signaling pathways and may contribute to N-Myc (zeige MYCN Antikörper)-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 (zeige CCNB1 Antikörper) gene expression.
These findings support MXI1 as a putative tumor suppressor gene involved in conventional melanoma progression.
Data show that PTEN (zeige PTEN Antikörper) 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 (zeige MYC Antikörper) family protein network acting as a dominant negative isoform of Mxi-F stimulated by c-Myc (zeige MYC Antikörper)
p300 (zeige EP300 Antikörper) can acetylate DNA-bound Myc:Max complexes and that acetylated Myc:Max heterodimers efficiently interact with Miz-1 (zeige ZBTB17 Antikörper)
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