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The mesangial cell apoptosis observed in this mesangial proliferative glomerulonephritis model was related to CXCL10 expression induced by Mxi1 inactivation.
Mxi1 regulates Ift20 promoter activity via Ets-1 binding to the Ift20 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.
down-regulation of miR-191 is essential for erythroid chromatin condensation and enucleation by allowing up-regulation of Riok3 and Mxi1
Mxi1-SRalpha is an isoform with enhanced transcriptional repression potential
Apolipoprotein A1 which is a major component of the high-density lipoprotein complex and has anti-inflammation effects, was significantly decreased in the Mxi1-deficient mouse.
a phosphorylation mutant form of Mxi1 (Mxi1-S160A), which cannot be degraded by S6K1 and beta-Trcp, is much more stable and efficient in suppressing the transcriptional activity of Myc and radioresistance in lung cancer cells.
Reactive oxygen species mediates hypoxia-induced VEGF by upregulation of Mxi1-0.
results suggest that Mxi1-0 regulates the growth of HUVECs via the IL-8 and ERK1/2 pathways, which apparently reciprocally activate each other
MYC-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-dependent signaling pathways and may contribute to N-Myc-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 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 family protein network acting as a dominant negative isoform of Mxi-F stimulated by c-Myc
p300 can acetylate DNA-bound Myc:Max complexes and that acetylated Myc:Max heterodimers efficiently interact with Miz-1
MXI1 mutation appears to play a role in the pathogenesis of a small subset of cases, and suggests an alternative mechanism to MYC amplification for disruption of the MYC/MAD/MAX network in medulloblastoma.
These results provide evidence of direct regulation of Mxi1 by FOXO3a and imply an additional mechanism through which the PI3-kinase/Akt/FOXO pathway can modulate Myc function.
Mad1, Mxi1 and Rox genes were expressed and displayed mutations in haematological malignancies.
Mxi1 gains functional complexity by encoding isoforms with shared and distinct activities
Missense mutations in Mad1, Mxi1 and Rox were found in acute leukemia patients.
Mxi1 is an important downstream target of HIF that contributes to pVHL-deficient renal cancer tumorigenesis
MAX interactor-1 (MXI1) gene is directly regulated by HIF-1alpha protein in neuroblastoma and breast cancer cells.
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