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Mutation of the MXI1 gene in prostate cancer. Paper-253684.
Mxi1 mutations in human neurofibrosarcomas. Paper-1965404.
Mice deficient for Mxi1 exhibit significant prostate hyperplasia. Paper-8838866.
Waiting for anaphase: Mad2 and the spindle assembly checkpoint. Paper-8604238.
Genomic organization of human MXI1, a putative tumor suppressor gene. Paper-845247.
Mxi1 also appears to lack a transcriptional activation domain. Paper-7924091.
Commonly occurring loss and mutation of the MXI1 gene in prostate cancer. Paper-1740433.
We examined 40 primary human pancreatic adenocarcinomas for MXI1 mutations. Paper-519478.
Inhibition of Mxi1 suppresses HIF-2alpha-dependent renal cancer tumorigenesis. Paper-13480339.
Our data demonstrate that mutations occur in the Mxi1 gene in neurofibrosarcoma. Paper-1965404.
Assignment of the human MAD and MXI1 genes to chromosomes 2p12-p13 and 10q24-q25. Paper-8173414.
The MXI1 tumor suppressor gene is not mutated in primary prostate cancer. Paper-1356190.
We subsequently isolated the MXI1 promoter, which is GC-rich and lacks a TATA box. Paper-8299461.
Mxi1 is a c-Myc antagonist and suppresses cell proliferation in vitro. Paper-11579917.
Mxi1-0, an alternatively transcribed Mxi1 isoform, is overexpressed in glioblastomas. Paper-11579917.
Mad2 overexpression promotes aneuploidy and tumorigenesis in mice. Paper-12424847.
Loss of heterozygosity in the MXI1 gene is a frequent occurrence in melanoma. Paper-10139083.
Mxi1 isoforms are expressed in hematological cell lines and normal bone marrow. Paper-10807788.
To explore mechanisms of Mxi1-induced growth arrest, we performed gene expression analysis. Paper-8838866.
Mxi1 tumor suppressor gene is not mutated in primary pancreatic adenocarcinoma. Paper-519478.
Localization of the human Mxi1 transcription factor gene ( MXI1) to chromosome 10q24-q25. Paper-8004236.
Spindle checkpoint component Mad2 contributes to biorientation of homologous chromosomes. Paper-10119515.
MXI1, a putative tumor suppressor gene, suppresses growth of human glioblastoma cells. Paper-1211315.
PTEN and MXI1 allelic loss on chromosome 10q is rare in melanoma in vivo. Paper-8325618.
Mxi1 is a Mad family member that plays a role in cell proliferation and differentiation. Paper-9392823.
In the present study we show that Mxi1 is overexpressed in primary human clear cell kidney cancers. Paper-13480339.
MXI1 maps to chromosome 10q24-q25, a region that is deleted in some cases of prostate cancer. Paper-253684.
Compared to Mxi1-proficient tumors, Mxi1-deficient tumors display reduced cellular proliferation. Paper-13480339.
HIF-1alpha induces MXI1 by alternate promoter usage in human neuroblastoma cells. Paper-14539309.
Therefore, Mxi1 and Mad might antagonize Myc function and are candidate tumor suppressor genes. Paper-7924091.
Four polymorphisms were found in cell lines BMMNC and PBMNC: two in Mad1, one in Mxi1 and one in Rox. Paper-13306687.
These results suggest that MXI1 is unlikely to play a role in human pancreatic adenocarcinoma tumorigenesis. Paper-519478.
Mxi1 is thought to negatively regulate Myc function and may therefore be a potential tumor suppressor gene. Paper-1965404.
Mad2 is an essential component of this checkpoint system and it binds specifically to unattached kinetochores. Paper-876966.
These findings support MXI1 as a putative tumor suppressor gene involved in conventional melanoma progression. Paper-10139083.
We show that the roles of two spindle checkpoint components, Mad2 and Mad3, differ in meiosis I. Paper-10119515.
Therefore, a substantial involvement of MXI1 gene alterations in the development of prostate cancer appears unlikely. Paper-1356190.
Furthermore, cell cycle analysis demonstrated that induction of MXI1 results in accumulation of cells in the G2-M phase. Paper-1211315.
Disruption of MAD2 expression leads to defects in the mitotic checkpoint, chromosome missegregation, and tumorigenesis. Paper-10648268.
Lack of deletions of the PTEN/ MMAC1 and MXI1 loci in renal cell carcinoma by interphase cytogenetics. Paper-2162488.
The MXI1 gene was mapped to human chromosome 10 at band q25 and on mouse chromosome 19 at region D by FISH. Paper-7924091.
Differential expression of c-myc, max and mxi1 in human myeloid leukemia cells during retrodifferentiation and cell death. Paper-431478.
The mxi1 mRNA increased during growth inhibition and differentiation, and decreased with serum stimulation in mammal cell lines. Paper-796053.
Furthermore, attempts to disable the function of the SAC protein, Mad2, in mouse oocytes have produced conflicting results. Paper-11078928.
We conclude that MXI1 gene loss in prostate cancer is common and most frequently involves a cytogenetically undetectable deletion. Paper-1740433.
In normal bone marrow and hematological cell lines, the dominantly expressed isoforms are Mxi-D and full-length Mxi1 (Mxi-F). Paper-10807788.
Consistent with these roles, mxi1 may be the tumour-suppressor gene that resides at region 24-26 of the long arm of chromosome 10. Paper-1444976.
MXI1 allelic loss was seen more frequently in recurrent/metastatic tumors (59%), as compared with in primary (33%) lesions. Paper-10139083.
Mxi1 inhibits the proliferation of U87 glioma cells through down-regulation of cyclin B1 gene expression. Paper-9392823.
Missense mutations in the functional domain of Mxi1 in these cases may be involved in the pathogenesis of neurofibrosarcoma. Paper-1965404.
To test the role of Mxi1 on tumorigenesis of glioma cells we transfected a CMV-driven MXI1 cDNA in U87 human glioblastoma cells. Paper-9392823.
The Mad2 protein is required to delay sister chromatid separation until all chromosomes have been aligned on the mitotic spindle. Paper-12029214.
One patient showed a metastatic tumor with allelic loss for MXI1 that was not identified in the primary melanoma or a local recurrence. Paper-10139083.
3. The MXI1 gene at 10q24-25 is another candidate tumor suppressor that has only rarely been studied in melanomas, with conflicting results. Paper-10139083.
BACKGROUND: Mxi1, an antagonist of c-Myc, maps to human chromosome 10q24-q25, a region altered in a substantial fraction of prostate tumors. Paper-8838866.
Human chromosomes 2p13 and 10q25 have been involved in specific tumors where the role of Mad and Mxi1 can now be investigated. Paper-7924091.
The MXI1 gene, located at 10q24-q25, may serve to negatively regulate c-myc oncogene activity, and potentially has tumor suppressor function. Paper-519478.
In the absence of Mad2, meiosis I nondisjunction occurs at a high frequency and can be corrected by delaying the onset of anaphase. Paper-10119515.
These results establish Mxi1 as an important downstream target of HIF that contributes to pVHL-deficient renal cancer tumorigenesis. Paper-13480339.
A candidate tumor suppressor gene from this region, Mxi1 at 10q25, has recently been shown to be mutated in a small number of prostate tumors. Paper-398879.
Correlation between methylation status and lack of expression was evident for PTEN, FGFR2, and MXI1 and was less clear for MGMT. Paper-13144573.
Mad family members, including Mad1, Mxi1, Mad3, Mad4, Mnt, and Mga, function in part as antagonists of Myc oncoproteins. Paper-11810015.
We prospectively evaluated prostate tumors for loss of MXI1 by fluorescence in situ hybridization (FISH) and cytogenetic techniques. Paper-1740433.
Moreover, continued overexpression of Mad2 is not required for tumor maintenance, unlike the majority of oncogenes studied to date. Paper-12424847.
Mxi1 protein is a basic helix-loop-helix, leucine zipper (bHLHZIP) transcriptional factor, which dimerizes with the Max protein. Paper-10807788.
We have reassessed the coding sequence of MXI1 and found that, at the 3' end, the open reading frame is 28 codons shorter than previously described. Paper-266806.
Bub1 has an upstream function in regulating the kinetochore localization of Mad2 and other downstream checkpoint components. Paper-11076762.
The absence of mutations in these genes suggested that FAS and MXI1 are not likely to be tumor suppressor genes physiologically relevant to GBM. Paper-1380089.
Mmipl is found in a variety of cells types, is induced by serum stimulation, and can be co-immunoprecipitated from fibroblasts in association with Mxi1. Paper-1375701.
Synchronization of proliferating U-937 cells throughout distinct phases of the cell cycle exhibited little, if any, change in c-myc, c-max and mxi1 mRNAs. Paper-431478.
Deletions in the long arm of chromosome 10 in lymphomas with t(14;18): a pathogenetic role of the tumor supressor genes PTEN/ MMAC1 and MXI1? Paper-1670452.
We report here the mapping of the MAD and MXI1 genes in human and mouse by fluorescence in situ hybridization (FISH) and by recombination mapping. Paper-7924091.
Fluorescence in situ hybridization also demonstrated loss of one MXI1 allele in an additional tumour lacking chromosome 10 abnormalities. Paper-253684.
In this report we show that the MAX interactor-1 ( MXI1) gene is directly regulated by HIF proteins in neuroblastoma and breast cancer cells. Paper-14539309.
We have recently reported a new link between an important cell cycle timer/regulator, MAD2, and the cytokine, stem cell factor, and its receptor. Paper-13130273.
The template model proposes that Mad1- Mad2 at kinetochores acts as a template to change the conformation of another binding molecule of Mad2. Paper-11199549.
This cancer-prone phenotype may correlate with the enhanced ability of several mxi1-deficient cell types, including prostatic epithelium, to proliferate. Paper-1444976.
New work highlights the importance of the Mad2- Mad2 interaction, and suggests how spindle checkpoint signals are propagated away from kinetochores. Paper-10733983.
Our results define a clear role for Mad2 in ensuring the proper timing of meiosis I events and ultimately, in ensuring the fidelity of homologue disjunction. Paper-11078928.
Nine missense mutations were detected: two in Mad1 in patients, four in Mxi1 (three in patients and one in KG-1 cell line), and three in Rox in patients. Paper-13306687.
MXI1, a member of the MYC family of transcription factors, is thought to negatively regulate MYC function and may therefore be a potential tumor suppressor gene. Paper-845247.
Sequence analysis revealed no somatic mutations in any of the six MXI1 coding exons, similar to findings in prostate tumors with MXI1 allelic loss. Paper-1211315.
Although Mxi1-0 and Mxi1 are coexpressed in both human and mouse cells, the relative levels of Mxi1-0 are higher in primary glioblastoma tumors than in normal brain tissue. Paper-11579917.
Because more than 90% of prostate tumors contain no cytogenetic abnormality of 10q, the relevance of MXI1 loss and/or mutation to the vast majority of cases remains unclear. Paper-1740433.
CONCLUSIONS: The ability of AdMxi1 to suppress prostate tumor cell proliferation supports a role for Mxi1 loss in the pathogenesis of a subset of human prostate cancers. Paper-8838866.
The correspondence of these exons to previously identified Mxi1 functional domains suggests that alternatively spliced transcripts may regulate Mxi1 functional activity. Paper-845247.
Using a combination of somatic cell mapping and fluorescence in situ hybridization techniques, we have determined the chromosomal locations of the MAD and MXI1 genes. Paper-8173414.
These studies provide further insight into the complex regulatory mechanisms governing MXI1 gene expression and its role in cellular differentiation and tumor suppression. Paper-8299461.
MXI1 thus displays allelic loss and mutation in some cases of prostate cancer that may contribute to the pathogenesis or neoplastic evolution of this common malignancy. Paper-253684.
The induction of Mxi1 by FOXO3a was specific to the Mxi1-SR alpha isoform and was mediated by three highly conserved FOXO binding sites within the first intron of the gene. Paper-13295281.
However, no mutations or homozygous deletions were found in the coding region of MXI1, a candidate tumor suppressor gene at 10q24-q25, in a panel of SCLC cell lines. Paper-1616657.
Finally, we have identified two polymorphic regions within the MXI1 locus: a polymorphic CA repeat in the third intron and an AAAAC polymorphism in the noncoding region of exon 6. Paper-845247.
Fifty-four percent (15 of 28) of the informative cases showed loss of heterozygosity for one or both MXI1 markers, as compared with 67% (16 of 24) of the informative cases for MTS1. Paper-10139083.
The MXI1 gene localizes to chromosome 10q24-q25, a region involved in translocations and deletions in acute and chronic lymphocytic leukemias and prostatic carcinomas. Paper-8173414.
We have also found an AAAAC polymorphic repeat in the 3' non-coding region of the human mxi1 cDNAs and a difference between the mxi1 mRNA half-lives in some different cell lines. Paper-796053.
Double mutant and inhibitor analyses revealed that Dis3 is required for correct kinetochore formation and function, and that this activity is monitored by the Mad2 checkpoint. Paper-12468621.
These proteins include the microtubule motors CENP-E and cytoplasmic dynein, and proteins involved with the mitotic spindle checkpoint, Mad2, Bub1R, and the 3F3/2 phosphoantigen. Paper-8889956.
We and others have previously mapped the MXI1 gene to the distal portion of chromosome 10q, a region that is rearranged or affected by allelic loss in many astrocytic brain tumors. Paper-1211315.
Thus, these studies support the notion that MXI1 normally functions to suppress cell growth and suggest that loss of MXI1 function may play a role in human glioblastoma development. Paper-1211315.
Taken together, these findings suggested differential regulation and inverse expression levels of c-myc compared to c-max and mxi1 during differentiation, retrodifferentiation and cell death. Paper-431478.
PICH contributes to the mitotic checkpoint by recruiting Mad2 to kinetochores and is proposed to regulate checkpoint signaling by monitoring tension at centromeres. Paper-12403805.
Using a newly described polymorphic CA microsatellite repeat in the third MXI1 intron, we show that 7 of 11 informative glioblastomas demonstrated MXI1 allelic loss. Paper-1211315.
Importantly, knock-down of MXI1 had limited effect on MYC/MYCN activity under hypoxia, an observation that might be related to the different functional attributes of the two MXI1 isoforms. Paper-14539309.
Also, postovulatory and in vitro aging of mouse oocytes has been shown to lead to decreased levels of Mad2 transcripts and elevated frequencies of premature centromere separation. Paper-12957654.
We also examined 29 human tumor cell lines consisting of 12 esophageal cancers, 7 glioma/ glioblastomas and 10 others for Mxi1 mutations in exons 1, 2, 4 (HLH domain), 5 and 6. Paper-1965404.
Our results show that Mxi1 is involved in the homeostasis of differentiated organ systems, acts as a tumour suppressor in vivo, and engages the Myc network in a functionally relevant manner. Paper-1444976.
These results demonstrate that transient Mad2 overexpression and chromosome instability can be an important stimulus in the initiation and progression of different cancer subtypes. Paper-12424847.
To gain further insight into SAC function during female mammalian meiosis I, we recently utilised a morpholino-based antisense approach to deplete the majority of Mad2 in mouse oocytes. Paper-11078928.
Inactivation of the MXI1 gene could, therefore, inhibit differentiation and enhance proliferation in the presence of normal levels of c-Myc, and thus MXI1 is a potential tumor suppressor gene. Paper-1211315.
Analysis of mouse mxi1 has led to the identification of two mxi1 transcript forms possessing open reading frames that differ in their capacity to encode a short amino-terminal alpha-helical domain. Paper-180096.
After clarification of the 5'- and 3'-untranslated regions of the cDNA (indicating that the true length of the MXI1 transcript is 2643 base pairs), we identified two transcription initiation sites. Paper-8299461.
Furthermore, suppression of spindle checkpoint function by BubR1 or Mad2 RNA interference in the DNA damaged cells led to escape from catastrophic death and to subsequent abnormal mitosis. Paper-10537055.
We screened the 10q locus for loss of heterozygosity and the promoter methylation status of PTEN, MGMT, MXI1, and FGFR2 in neuroblastic tumors and neuroblastoma cell lines. Paper-13144573.
In addition, we utilized SSCP analysis to test two other candidate genes on 10q: FAS, a cell surface receptor which transduces an apoptotic, cell death signal and MXI1, a transcriptional repressor. Paper-1380089.
Accurate chromosome segregation in meiosis I depends on spindle checkpoint proteins such as Mad2 which delay APC/C activation in response to an erroneous spindle attachment of chromosomes. Paper-11368198.
MXI1 encodes a basic-helix-loop-helix protein that suppresses the transcriptional activity of the MYC oncoprotein by competing for the common dimerization partner, MAX, and binding to identical DNA sites. Paper-1740433.
Mxi1, a c-Myc antagonist, is a HIF target gene that inhibits mitochondrial biogenesis, reprograms cellular energy metabolism, and protects cells from c-Myc-dependent apoptosis in vitro. Paper-13480339.
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. Paper-12320459.
Inhibition of Mxi1 in pVHL-defective kidney cancer cells using shRNA alters their cell cycle parameters, inhibits their ability to invade matrigel, and suppresses their ability to form tumors in vivo. Paper-13480339.
The distal long arm of chromosome 10 harbors genes of biomedical interest such as MXI1, a putative tumor suppressor gene, and those encoding the adrenergic receptors alpha2A (ADRA2A) and beta1 ( ADRB1). Paper-1300952.
Mapping of two genes encoding members of a distinct subfamily of MAX interacting proteins: MAD to human chromosome 2 and mouse chromosome 6, and MXI1 to human chromosome 10 and mouse chromosome 19. Paper-7924091.
Furthermore, Mad2 up-regulation in these cells suggested that overexpression of spindlin1 may affect the bipolar spindle correctly attachment to chromosomes and activate spindle checkpoint. Paper-12920726.
Two Developmental Cell papers in this issue by Kulukian et al. and Malureanu et al. now provide insight into how checkpoint components Mad2 and BubR1 relay the checkpoint signal from kinetochores to APC/C. Paper-13581995.
The MXI1 gene encodes a protein interacting with Max, a regulatory factor of the Myc oncogene, and is located on chromosome 10q25, a region showing frequent loss of heterozygosity in malignant gliomas. Paper-266806.
Furthermore, like c-myc, c-max and mxi1 mRNA transcripts appeared to be regulated primarily by post-transcriptional mechanisms, and c-max and mxi1 half-lives exceeded 4 h in contrast to < 60 min for the c-myc gene. Paper-431478.
Thus, our findings indicate that Mxi1 can act as a tumour suppressor in human glioblastomas through a molecular mechanism involving the transcriptional down-regulation of cyclin B1 gene expression. Paper-9392823.
MAD2 is localized to kinetochores of unaligned chromosomes, where it inactivates the anaphase-promoting complex/cyclosome, thus contributing to the production of a diffusible anaphase inhibitory signal. Paper-10648268.
Reducing the levels of the checkpoint proteins BubR1 or Mad2 in human cancer cells or inhibiting BubR1 kinase activity provokes apoptotic cell death within six divisions except when cytokinesis is also inhibited. Paper-10345444.
Redefinition of the coding sequence of the MXI1 gene and identification of a polymorphic repeat in the 3' non-coding region that allows the detection of loss of heterozygosity of chromosome 10q25 in glioblastomas. Paper-266806.
The Mxi1 protein functions in a regulatory network with members of the c-Myc family, in which c-Myc activates transcription and stimulates cell proliferation, and Mxi1 negatively regulates these actions. Paper-1211315.
Several serum deprivation early response genes (SDERGs), including the putative tumor suppressor genes SALL2 and MXI1, are required for cessation of DNA synthesis in response to SD and induction of additional SD genes. Paper-13378668.
METHODS: We infected DU145 prostate carcinoma cells with an Mxi1-expressing adenovirus (AdMxi1) in vitro, and measured Mxi1 expression, cell proliferation, soft agar colony formation, and cell cycle distribution. Paper-8838866.
For prostate cancer, allelic deletions from the long arm of chromosome 10 (#10q23-25), the locus of the putative tumor suppressor gene MXI1 (#10q24-25), have been identified as a frequently occurring genetic event. Paper-1356190.
In different organisms, a mitotic checkpoint complex (MCC) composed of Mad2, Bub3, BubR1/ Mad3, and Cdc20 inhibits the anaphase promoting complex ( APC/C) to initiate promotion into anaphase. Paper-13491278.
Mad2 is an essential component of the spindle checkpoint that blocks activation of Separase and dissolution of sister chromatids until microtubule attachment to kinetochores is complete. Paper-12424847.
When bound to DNA by a LexA moiety in yeast, Mxi1 does not stimulate transcription. mxi1 mRNA is expressed in many tissues, and its expression is elevated in U-937 myeloid leukemia cells that have been stimulated to differentiate. Paper-81701.
These findings implicate the inactivation of critical TS loci at 10q23.3-25.3 in medulloblastoma, however comprehensive analysis of SUFU, BTRC and MXI1 indicates they are unlikely to represent major targets of these allelic losses. Paper-12320459.
Between 7 and 11 days of TPA-induced G0/G1 cell cycle arrest, expression of the c-max and mxi1 genes continuously increased up to 8-fold until 32 days and declined to control levels when the cells regained proliferative capacity by 36 days. Paper-431478.
Due to the detection of point mutations in the retained alleles of four primary adenocarcinomas of the prostate, MXI1 gene alterations have been suggested to be involved in the development and/or the progression of prostate cancer. Paper-1356190.
The identification of Mxi1-0 as an alternatively transcribed Mxi1 isoform has significant implications for the interpretation of previous Mxi1 studies, particularly those related to the phenotype of the mxi1 knockout mouse. Paper-11579917.
To determine whether MXI1 can indeed function as a suppressor of growth, we have introduced a steroid-inducible MXI1 expression vector into the U87MG cell line, a glioblastoma cell line lacking endogenous MXI1 expression. Paper-1211315.
Dynein/dynactin inhibition did not block chromosome congression to the spindle equator in prometaphase, or segregation to the poles in anaphase when the spindle checkpoint was inactivated by microinjection with Mad2 antibodies. Paper-8889956.
Treatment of U-937 cells with 12-O-tetradecanoyl phorbol-13-acetate (TPA) which is associated with the induction of a monocytic differentiation program and growth arrest, revealed an initial up-regulation of c-myc, c-max, and mxi1 mRNAs after 1-6 h. Paper-431478.
3. This region contains three genes, MXI1, SUFU and BTRC, which represent putative medulloblastoma tumor suppressor (TS) genes on the basis of either (i) negative regulation of critical medulloblastoma pathways, or (ii) mutation in other cancer types. Paper-12320459.
Although a consistent pattern did not emerge among the markers, LOH of 9p21 (D9S254) occurred in 60% (9/15) of the cases followed by 40% of cases displaying LOH of 1p34, p53, 10q ( MXI1), and 10q23 (D10S520) and 25% with 5q21 (D5S 592) abnormalities. Paper-9707622.
HIF-binding and transactivation were detected within MXI1 gene regulatory sequences in the vicinity of the MXI1-0 promoter, leading to rapid induction of the alternate MXI1-0 isoform followed by a long-term induction of both the MXI1-0 and MXI1 isoforms. Paper-14539309.
Through binding to its target Cdc20, Mad2 inhibits the multisubunit ubiquitin ligase, the anaphase-promoting complex or cyclosome ( APC/C), and delays the onset of anaphase until all sister chromatids achieve bipolar attachment to the mitotic spindle. Paper-13089509.
We show here that overexpression of Mad2 in transgenic mice leads to a wide variety of neoplasias, appearance of broken chromosomes, anaphase bridges, and whole-chromosome gains and losses, as well as acceleration of myc-induced lymphomagenesis. Paper-12424847.
This observation suggests that Mad2 plays a role in reorienting chromosomes that are incorrectly attached to the spindle as well as delaying the cell cycle, whereas Mad3 is needed for the cell cycle delay, but not for chromosome reorientation. Paper-10119515.
The Myc antagonists Mad1, Mxi1 and Rox proteins share two highly conserved domains, Sin3-interacting domain ( SID) and basic helix-loop-helix leucine zipper domain (bHLHzip), which are essential for these proteins to function during molecular switching from proliferation to differentiation. Paper-13306687.
We next identified and characterised CpG islands associated with 5' regions of the MXI1, SUFU and BTRC genes; analysis of these regions for evidence of DNA hypermethylation, alongside expression analysis of their respective transcripts, revealed no evidence to support epigenetic inactivation of any gene. Paper-12320459.
These synonyms are used for gene MXI1 (MAX interactor 1): MXI, MXD2, MGC43220, Max interactor 1, Max-interacting protein 1, MAD2, Class C basic helix-loop-helix protein 11, BHLHC11, bHLHc11.
These accession numbers are used for gene MXI1: Q15887 (UNIPROT__AC), D3DR25 (UNIPROT__AC), CR594058 (NCBI_GENBANK__AC), AK309718 (NCBI_GENBANK__AC).
MXI1 is a homologue of MXI1 (MAX interactor 1) from Pan troglodytes.
MXI1 is a homologue of MXI1 (MAX interactor 1) from Canis lupus familiaris.
MXI1 is a homologue of MXI1 (MAX interactor 1) from Bos taurus.
MXI1 is a homologue of MXI1 (MAX interactor 1) from Gallus gallus.
MXI1 is a homologue of Mxi1 (Max interacting protein 1) from Mus musculus.
MXI1 is a homologue of mxi1 (max interacting protein) from Danio rerio.
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