MLXIPL

From Wikipedia, the free encyclopedia

MLX interacting protein-like

Identifiers

MLXIPL; CHREBP; MIO; MONDOB; WBSCR14; WS-bHLH

External IDs

OMIM: 605678 MGI: 1927999 HomoloGene: 32507

Gene ontology
Molecular Function:	• DNA binding • transcription repressor activity
Cellular Component:	• nucleus • transcription factor complex
Biological Process:	• negative regulation of transcription from RNA polymerase II promoter • regulation of transcription, DNA-dependent • anatomical structure morphogenesis

RNA expression pattern

More reference expression data

Orthologs

Human

Mouse

Refseq

NM_032951 (mRNA)
NP_116569 (protein)

NM_021455 (mRNA)
NP_067430 (protein)

Location

Chr 7: 72.65 - 72.68 Mb

Chr 5: 135.39 - 135.42 Mb

Pubmed search

[1]

[2]

MLX interacting protein-like, also known as MLXIPL, is a human gene.^[1]

This gene encodes a basic helix-loop-helix leucine zipper transcription factor of the Myc/Max/Mad superfamily. This protein forms a heterodimeric complex and binds and activates, in a glucose-dependent manner, carbohydrate response element (ChoRE) motifs in the promoters of triglyceride synthesis genes. The gene is deleted in Williams-Beuren syndrome, a multisystem developmental disorder caused by the deletion of contiguous genes at chromosome 7q11.23.^[1]

[edit] References

^ ^a ^b Entrez Gene: MLXIPL MLX interacting protein-like.

[edit] Further reading

Meng X, Lu X, Li Z, et al. (1999). "Complete physical map of the common deletion region in Williams syndrome and identification and characterization of three novel genes.". Hum. Genet. 103 (5): 590-9. PMID 9860302.
de Luis O, Valero MC, Jurado LA (2000). "WBSCR14, a putative transcription factor gene deleted in Williams-Beuren syndrome: complete characterisation of the human gene and the mouse ortholog.". Eur. J. Hum. Genet. 8 (3): 215-22. doi:10.1038/sj.ejhg.5200435. PMID 10780788.
Cairo S, Merla G, Urbinati F, et al. (2001). "WBSCR14, a gene mapping to the Williams--Beuren syndrome deleted region, is a new member of the Mlx transcription factor network.". Hum. Mol. Genet. 10 (6): 617-27. PMID 11230181.
Kawaguchi T, Takenoshita M, Kabashima T, Uyeda K (2002). "Glucose and cAMP regulate the L-type pyruvate kinase gene by phosphorylation/dephosphorylation of the carbohydrate response element binding protein.". Proc. Natl. Acad. Sci. U.S.A. 98 (24): 13710-5. doi:10.1073/pnas.231370798. PMID 11698644.
Kawaguchi T, Osatomi K, Yamashita H, et al. (2002). "Mechanism for fatty acid "sparing" effect on glucose-induced transcription: regulation of carbohydrate-responsive element-binding protein by AMP-activated protein kinase.". J. Biol. Chem. 277 (6): 3829-35. doi:10.1074/jbc.M107895200. PMID 11724780.
Strausberg RL, Feingold EA, Grouse LH, et al. (2003). "Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences.". Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899-903. doi:10.1073/pnas.242603899. PMID 12477932.
Ota T, Suzuki Y, Nishikawa T, et al. (2004). "Complete sequencing and characterization of 21,243 full-length human cDNAs.". Nat. Genet. 36 (1): 40-5. doi:10.1038/ng1285. PMID 14702039.
Hillman RT, Green RE, Brenner SE (2005). "An unappreciated role for RNA surveillance.". Genome Biol. 5 (2): R8. doi:10.1186/gb-2004-5-2-r8. PMID 14759258.
Merla G, Howald C, Antonarakis SE, Reymond A (2005). "The subcellular localization of the ChoRE-binding protein, encoded by the Williams-Beuren syndrome critical region gene 14, is regulated by 14-3-3.". Hum. Mol. Genet. 13 (14): 1505-14. doi:10.1093/hmg/ddh163. PMID 15163635.
Gerhard DS, Wagner L, Feingold EA, et al. (2004). "The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC).". Genome Res. 14 (10B): 2121-7. doi:10.1101/gr.2596504. PMID 15489334.
Li MV, Chang B, Imamura M, et al. (2006). "Glucose-dependent transcriptional regulation by an evolutionarily conserved glucose-sensing module.". Diabetes 55 (5): 1179-89. PMID 16644671.