Disease relevance of Atp10a

• The localization of Atp10a neighboring the maternally expressed gene Ube3a in the imprinted domain and an unusual inheritance pattern of the obesity phenotype with a p-locus deletion have suggested that Atp10a might be imprinted and associated with body fat [1].

High impact information on Atp10a

• Although sex differences were observed, our data suggest that heterozygous deletion along with an unusual pattern of maternal inheritance of the chromosomal region containing the single gene, Atp10c, causes obesity, type 2 diabetes, and nonalcoholic fatty liver disease in these mice [2].
• The purpose of this study was to assess the overall effect of the heterozygous deletion of Atp10c on obesity-related phenotypes and metabolic abnormalities in mice fed a high-fat diet [2].
• Atp10c is a novel type IV P-type ATPase and is a putative phospholipid transporter [2].
• The mouse Atp10a gene is located at the border of an imprinted domain distal to the p-locus on mouse chromosome 7 [1].
• These findings suggest that the mouse Atp10a gene escapes genomic imprinting [1].

Biological context of Atp10a

• A putative promoter region of PFATP contains a strong CpG island [3].
• Full-length cDNA was generated, and the corresponding genomic structure was deduced from the Human Genome Database. RESULTS: Murine pfatp, and its human ortholog, PFATP, belong to class V of the third subfamily of P-type ATPases [3].

Anatomical context of Atp10a

• Predominant maternal expression of the mouse Atp10c in hippocampus and olfactory bulb [4].
• This gene, which we have called p-locus fat-associated ATPase (pfatp) is differentially expressed in human and mouse tissues with predominant expression in the testis and lower levels of expression in adipose tissue and other organs [5].
• The most striking observation is the loss of Atp10c expression in the mutants, specifically in the soleus muscle, after eating the high-fat diet for 12 weeks [6].
• The expression of Atp10c is also significantly altered in the adipose tissue and the soleus muscle [6].

Associations of Atp10a with chemical compounds

• Adipose tissue and the skeletal muscle are the targets, and GLUT4-mediated glucose uptake is the specific metabolic pathway associated with Atp10c deletion [6].

References