ACBD7
- Known as:
- ACBD7
- Catalog number:
- 000993A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACBD7
Related genes to: ACBD7
- Gene:
- ACBD7 NIH gene
- Name:
- acyl-CoA binding domain containing 7
- Previous symbol:
- -
- Synonyms:
- FLJ38219, bA455B2.2
- Chromosome:
- 10p13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-27
- Date modifiied:
- 2019-03-21
Related products to: ACBD7
Related articles to: ACBD7
- Understanding the molecular basis of hair cell function is essential for elucidating inner ear physiology and developing therapies for auditory-vestibular disorders. Here, we identify acyl-CoA binding domain-containing 7 (Acbd7) as a hair cell-specific gene critical for sensory maintenance. Single-cell transcriptomics of mouse cochlear organoids revealed Acbd7 as a top hair cell-enriched transcript, with its spatiotemporal expression confirmed from embryonic development through adulthood in both auditory and vestibular hair cells. Acbd7‑deficient mice exhibited pronounced hair cell degeneration, characterized by synaptic defects and diminished calcium currents in inner hair cells and loss of outer hair cells. Transcriptomic and proteomic analyses linked Acbd7 to the regulation of Ca signaling and fatty acid metabolism pathways. Our findings establish Acbd7 as a critical regulator of Ca homeostasis and functional integrity in hair cells, thereby elucidating a key mechanism by which a fatty acid metabolism factor sustains hair cell function and providing potential therapeutic targets for inner ear disorders. - Source: PubMed
Publication date: 2026/08/14
Wu MingxuanJia GaoganJia YanyanHuang YikangLi YunjieLiu YaoqianLou YiyunSun TianshiQiu XintongXia MingyuLi HuaweiLi Wenyan - Altered lipid metabolism is increasingly recognized as a driver of tumor progression, yet its specific role in thyroid cancer remains unclear. - Source: PubMed
Publication date: 2026/05/17
Wang TianzeNan BoyuanSa QilaXu NingZhang Wei - We sequenced and assembled using multiple long-read sequencing technologies the genomes of chimpanzee, bonobo, gorilla, orangutan, gibbon, macaque, owl monkey, and marmoset. We identified 1,338,997 lineage-specific fixed structural variants (SVs) disrupting 1,561 protein-coding genes and 136,932 regulatory elements, including the most complete set of human-specific fixed differences. We estimate that 819.47 Mbp or ∼27% of the genome has been affected by SVs across primate evolution. We identify 1,607 structurally divergent regions wherein recurrent structural variation contributes to creating SV hotspots where genes are recurrently lost (e.g., CARD, C4, and OLAH gene families) and additional lineage-specific genes are generated (e.g., CKAP2, VPS36, ACBD7, and NEK5 paralogs), becoming targets of rapid chromosomal diversification and positive selection (e.g., RGPD gene family). High-fidelity long-read sequencing has made these dynamic regions of the genome accessible for sequence-level analyses within and between primate species. - Source: PubMed
Publication date: 2024/02/29
Mao YafeiHarvey William TPorubsky DavidMunson Katherine MHoekzema KendraLewis Alexandra PAudano Peter ARozanski AllisonYang XiangyuZhang ShilongYoo DongAhnGordon David SFair TylerWei XiaoxiLogsdon Glennis AHaukness MarinaDishuck Philip CJeong HyeonsooDel Rosario RicardoBauer Vanessa LFattor Will TWilkerson Gregory KMao YuxiangShi YongyongSun QiangLu QingPaten BenedictBakken Trygve EPollen Alex AFeng GuopingSawyer Sara LWarren Wesley CCarbone LuciaEichler Evan E - To study the diagnostic value of mRNA expression in urinary exocrine body in bladder cancer. - Source: PubMed
Publication date: 2024/02/23
Wang XinyingSong DianbinZhu BaoxingJin YangCai CaisenWang Zhiyong - Anorexia nervosa (AN) is a severe psychiatric disorder characterized by an intense fear of gaining weight, a relentless pursuit of thinness, and a distorted body image. Recent research highlights the substantial contribution of genetics to AN's etiology, with genes like BDNF, SLC6A4, and DRD2 implicated. However, a comprehensive genetic test for AN diagnosis is lacking. This study aims to elucidate the biological foundations of AN, examining variants in genes associated with syndromic forms, rare variants in AN patients, and candidate genes from GWAS studies, murine models, or established molecular pathways. - Source: PubMed
Donato KMedori M CMacchia ACecchin SCeccarini M RBeccari TGatta VStuppia LBenfatti VDalla Ragione LMicheletti P Chiurazzi CDhuli KMadeo GBonetti GMarceddu GBertelli M