ATP10D
- Known as:
- ATP10D
- Catalog number:
- 002267A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATP10D
Related genes to: ATP10D
- Gene:
- ATP10D NIH gene
- Name:
- ATPase phospholipid transporting 10D (putative)
- Previous symbol:
- -
- Synonyms:
- ATPVD, KIAA1487
- Chromosome:
- 4p12
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-25
- Date modifiied:
- 2016-06-28
Related products to: ATP10D
Related articles to: ATP10D
- C57BL/6J mice are widely used in biomedical research and are susceptible to insulin resistance and dyslipidemia when challenged with high fat diets relative to other inbred strains. Interestingly, C57Bl/6J mice contain a naturally occurring premature termination codon in the lipid flippase Atp10D, and previous studies have linked Atp10D to the metabolic disease-prone phenotype in mice and atherosclerotic severity in humans. In this study, we used CRISPR/Cas9 to revert the premature termination codon to the wild-type glutamine codon (Atp10D *817Q) in the C57Bl/6J mouse strain. The RNA transcripts from original and corrected alleles are dually expressed in heterozygous mice, suggesting that the mutant transcript escapes nonsense-mediated decay. Expression of two corrected Atp10D alleles restores wildtype expression levels of the transcript and protein in the liver. When challenged with a high fat diet, Atp10D (original) and Atp10D (corrected) C57Bl/6J mice showed no significant difference in weight gain, glucose tolerance, or plasma levels of triglycerides, cholesterol, or free fatty acids. However, the female Atp10D mice displayed an increase in complex glycosphingolipids and a reduction in cardiolipins in the plasma. These results suggest that restoring the expression of Atp10D in C57Bl/6J mice does not reverse insulin resistance and dyslipidemia in response to high fat diet feeding. - Source: PubMed
Publication date: 2026/07/07
Mansueto Alexander JNorris Adriana CYazlovitskaya Eugenia MZhu LinLu JoeyKoomen David CMay Jody CKim MinsooHermanson Jake NMolday Robert SMcLean John APlate LarsStafford John MGraham Todd R - GBA1 variants and decreased glucocerebrosidase activity are implicated in Parkinson's disease (PD). We investigated the hypothesis that increased levels of glucosylceramide (GlcCer), a main substrate of glucocerebrosidase, are involved in PD pathogenesis. Using multiple genetic methods, we show that ATPase phospholipid transporting 10D (ATP10D), not GBA1, is the main regulator of plasma GlcCer levels, yet it is not involved in PD pathogenesis. Plasma GlcCer levels were associated with PD, but not in a causative manner, and are not predictive of disease status. These results argue against targeting GlcCer in GBA1-PD, and underscore the need to explore alternative mechanisms and biomarkers for PD. ANN NEUROL 2025;97:873-878. - Source: PubMed
Publication date: 2025/03/01
Somerville Emma NJames AlvaBeetz ChristianSchwieger RobertBarrel GalKandaswamy Krishna KIurascu Marius IBauer PeterTa MichaelIwaki HirotakaSenkevich KonstantinYu EricAlcalay Roy NGan-Or Ziv - variants and decreased glucocerebrosidase (GCase) activity are implicated in Parkinson's disease (PD). We investigated the hypothesis that increased levels of glucosylceramide (GlcCer), one of GCase main substrates, are involved in PD pathogenesis. Using multiple genetic methods, we show that not , is the main regulator of plasma GlcCer levels, yet it is not involved in PD pathogenesis. Plasma GlcCer levels were associated with PD, but not in a causative manner, and are not predictive of disease status. These results argue against targeting GlcCer in -PD and underscore the need to explore alternative mechanisms and biomarkers for PD. - Source: PubMed
Publication date: 2024/09/16
Somerville Emma NJames AlvaBeetz ChristianSchwieger RobertBarrel GalKandaswamy Krishna KIurascu Marius IBauer PeterTa MichaelIwaki HirotakaSenkevich KonstantinYu EricAlcalay Roy NGan-Or Ziv - Global discovery lipidomics can provide comprehensive chemical information toward understanding the intricacies of metabolic lipid disorders such as dyslipidemia; however, the isomeric complexity of lipid species remains an analytical challenge. Orthogonal separation strategies, such as ion mobility (IM), can be inserted into liquid chromatography-mass spectrometry (LC-MS) untargeted lipidomic workflows for additional isomer separation and high-confidence annotation, and the emergence of high-resolution ion mobility (HRIM) strategies provides marked improvements to the resolving power ( > 200) that can differentiate small structural differences characteristic of isomers. One such HRIM strategy, high-resolution demultiplexing (HRdm), utilizes multiplexed drift tube ion mobility spectrometry (DTIMS) with post-acquisition algorithmic deconvolution to access high IM resolutions while retaining the measurement precision inherent to the drift tube technique; however, HRdm has yet to be utilized in untargeted studies. In this manuscript, a proof-of-concept study using ATP10D dysfunctional murine models was investigated to demonstrate the utility of HRdm-incorporated untargeted lipidomic analysis pipelines. Total lipid features were found to increase by 2.5-fold with HRdm compared to demultiplexed DTIMS as a consequence of more isomeric lipids being resolved. An example lipid, PC 36:5, was found to be significantly higher in dysfunctional ATP10D mice with two resolved peaks observed by HRdm that were absent in both the functional ATP10D mice and the standard demultiplexed DTIMS acquisition mode. The benefits of utilizing HRdm for discerning isomeric lipids in untargeted workflows have the potential to enhance our analytical understanding of lipids related to disease complexity and biologically relevant studies. - Source: PubMed
Publication date: 2024/09/14
Koomen David CMay Jody CMansueto Alexander JGraham Todd RMcLean John A - Over 8% of couples worldwide are affected by infertility and nearly half of these cases are due to male-specific issues where the underlying cause is often unknown. Therefore, discovery of new genetic factors contributing to male-specific infertility in model organisms can enhance our understanding of the etiology of this disorder. Here we show that murine ATP10A, a phospholipid flippase, is highly expressed in male reproductive organs, specifically the testes and vas deferens. Therefore, we tested the influence of ATP10A on reproduction by examining fertility of knockout mice. Our findings reveal that deficiency leads to male-specific infertility, but does not perturb fertility in the females. The deficient male mice exhibit smaller testes, reduced sperm count (oligozoospermia) and lower sperm motility (asthenozoospermia). Additionally, deficient mice display testes and vas deferens histopathological abnormalities, as well as altered total and relative amounts of hormones associated with the hypothalamic-pituitary-gonadal axis. Surprisingly, circulating testosterone is elevated 2-fold in the knockout mice while luteinizing hormone, follicle stimulating hormone, and inhibin B levels were not significantly different from WT littermates. The knockout mice also exhibit elevated levels of gonadotropin receptors and alterations to ERK, p38 MAPK, Akt, and cPLA-dependent signaling in the testes. was knocked out in the C57BL/6J background, which also carries an inactivating nonsense mutation in the closely related lipid flippase, We have corrected the nonsense mutation using CRISPR/Cas9 and determined that loss of alone is sufficient to cause infertility in male mice. Collectively, these findings highlight the critical role of ATP10A in male fertility in mice and provide valuable insights into the underlying molecular mechanisms. - Source: PubMed
Publication date: 2024/02/13
Norris Adriana CYazlovitskaya Eugenia MYang Tzushan SharonMansueto AlexStafford John MGraham Todd R