Ask about this productRelated genes to: ABCC9 antibody
- Gene:
- ABCC9 NIH gene
- Name:
- ATP binding cassette subfamily C member 9
- Previous symbol:
- -
- Synonyms:
- SUR2, CMD1O
- Chromosome:
- 12p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2019-04-23
Related products to: ABCC9 antibody
Related articles to: ABCC9 antibody
- ATP-sensitive potassium (KATP) channels are among the most expressed ion channels in skeletal muscle sarcolemma. While all KATP subunits can be detected in skeletal muscles, transcripts are enriched for KCNJ11 and ABCC9, suggesting that noncanonical Kir6.2/SUR2A assembly may constitute the majority of sarcolemmal KATP channels, but there has been no systematic dissection of KATP makeup in skeletal muscles. Here, we used a unique collection of murine lines selectively lacking specific channel-forming subunits (knockout, KO), and combined a genetic and pharmacological approach to determine which subunits of KATP channels are functionally relevant for skeletal muscle contraction. Under fatiguing conditions, isometric tetanic contraction experiments on murine extensor digitorum longus (EDL) revealed delayed loss of stimulated forces, and significant development of unstimulated forces, in muscles lacking Kir6.2 or SUR2 subunits, whereas loss of the SUR1 subunit did not impact muscle functionality. While pharmacological inhibition of sarcolemmal channels with glibenclamide causes comparable development of unstimulated force in wild-type muscles, acute pharmacological modulators of sarcolemmal KATP channels in isolated Kir6.2 or SUR2 KO muscles resulted in no changes in contractility properties, further consistent with no additional sarcolemmal KATP channels including Kir6.1 or SUR1 subunits. Our data show that fast-twitch skeletal muscle EDL relies on functional noncanonical KATP channels only made by ABCC9 (SUR2) and KCNJ11 (Kir6.2) gene products for contraction and suggest that similar contractile deficits will be present in ABCC9-dependent intellectual disability myopathy syndrome and KCNJ11-dependent congenital hyperinsulinism. - Source: PubMed
Publication date: 2026/05/20
Scala RosaChen YuezhouMizrak BerkMeyer Gretchen ANichols Colin G - The inflammatory response is a direct factor leading to changes in the microenvironment of renal tissues. The immune cells and stromal cells infiltration were the essential characteristics of diabetic nephropathy (DN). Based on the differentiation of the microenvironment, describing the heterogeneity of DN may provide a new approach to explore the mechanisms of disease progression. This study was aimed to classify DN samples based on the infiltration levels of immune cells and stromal cells, describe the microenvironment heterogeneity of DN samples, explore the potential mechanisms of phenotypic differentiation, screen key pathogenic genes, construct a quantitative scoring model to describe the microenvironment, and investigate the role of key pathogenic genes of DN. We downloaded RNA sequencing datasets of DN tissue and normal kidney tissue (GSE142025 and GSE96804) from the Gene Expression Omnibus (GEO) database. The RNA sequencing data was transformed into immune cell and stromal cell infiltration data using the xCell algorithm. Ward's method was used for consensus clustering to identify different phenotypes of DN. We screened out the key pathogenic genes associated with phenotypes, and established a scoring model through principal component analysis which was tested the reliability and accuracy in the training cohort and the validation cohort. We explored the influence of key pathogenic genes on the biological behavior of human mesangial cells. Based on the heterogeneity of the diabetic nephropathy (DN) microenvironment, this study identified 15 key pathogenic genes: FN1, EGR1, TPM1, CCND2, COL1A2, TGFB2, COL6A3, ITGA11, ABCC9, THBS2, TNC, COL3A1, C7, C1QC, and ITGB6. The PCA score constructed from these genes (i.e., their first principal component, PC1) demonstrated good efficacy in distinguishing normal samples from DN samples (AUC = 0.90, 95 % CI [0.82-0.97]), differentiating DN subtypes with distinct microenvironments (AUC = 0.99, 95 % CI [0.97-1.00]), and stratifying DN samples at different disease stages. This score showed significant positive correlations with immune score (r = 0.75, = 1.6e-7) and stromal score (r = 0.96, < 2.2e-16). Under high-glucose stimulation, the protein and mRNA expression of ABCC9 in mesangial cells increased over time. Knockdown of ABCC9 partially counteracted the high glucose-induced increase in apoptosis and enhancement of migration in mesangial cells. In an external validation cohort, both the PCA score (AUC = 0.91 for distinguishing normal from DN; AUC = 0.95 for differentiating DN subtypes) and ABCC9 expression (AUC = 0.93 for distinguishing normal from DN; AUC = 0.90 for distinguishing early from advanced DN) further confirmed their association with the DN microenvironment and disease progression. FN1, EGR1, TPM1, CCND2, COL1A2, TGFB2, COL6A3, ITGA11, ABCC9, THBS2, TNC, COL3A1, C7, C1QC, and ITGB6 are potential key pathogenic genes in DN. The PCA score constructed based on these genes can distinguish between normal tissue phenotype and DN phenotype, quantitatively describing the immune microenvironment and stromal microenvironment of DN, reflecting the progression of DN. Knocking out ABCC9 can counteract the increased apoptosis and migration of glomeruli mesangial cells induced by high glucose. - Source: PubMed
Publication date: 2026/04/17
Tan MiaoXue JingjingTan JinchuanRen MeifangZhang QianChen SuzhiSong RuijingNui YuhanZhao YicongLi YongzhangYang Fengwen - Adenosine triphosphate (ATP)-sensitive potassium cardiac channels (K) are composed of inward rectifying potassium channel (Kir) subunit Kir6.1 or Kir6.2, encoded by KCNJ8 or KCNJ11, and the sulfonylurea receptor SUR2 or SUR1, encoded by ABCC9 or ABCC8. - Source: PubMed
Publication date: 2026/04/16
Hu DanHuang YanRangel-Sandoval CinthiaSánchez-Pastor EnriqueOnetti Carlos GFerrer-Villada TaniaJiang Meng-NanHasdemir CanAkin IbrahimZhou Xiao-BoEl-Battrawy IbrahimCui MengRomano JohnPinheiro MariahAcuña-Ochoa Jose GChen LiangZhuang Le-NanHao Guo-LiangZhan Li-YingJiang HongAntzelevitch CharlesBarajas-Martínez Hector - Glycolysis plays a critical role in regulatory T cells (Tregs), which are frequently exploited by tumor cells, as Treg survival depends on glycolytic activity to suppress antitumor immunity. However, the precise effects of glycolysis on Treg proliferation and differentiation remain incompletely understood. Monocarboxylate transporters (MCTs) are pivotal regulators of glycolytic flux. In this study, we investigated how MCT1 inhibition modulates Treg metabolism and function, and the potential implications for tumor immunotherapy. Silencing MCT1 in human primary Tregs using siRNA disrupted glycolysis, leading to G0/G1 cell cycle arrest, increased apoptosis, and ATP depletion. Integrated metabolomic and transcriptomic analyses identified the ABC transporter pathway as the most significantly altered, with coordinated changes in key genes (ABCA1, ABCB10, ABCC9, etc.) and the metabolite adenosine. Validation using The Cancer Genome Atlas (TCGA) acute myeloid leukemia cohort demonstrated that high expression of the ABC transporter gene ABCC9 is associated with improved overall survival (hazard ratio = 0.45, p < 0.001). These findings indicate that MCT1 inhibition is associated with alterations in the ABC transporter pathway, which may correlate with changes in Treg metabolism and the tumor immune microenvironment. Collectively, this work highlights metabolic reprogramming of Tregs as a novel therapeutic target for cancer immunotherapy. - Source: PubMed
Publication date: 2026/03/09
Wang ZiyuWang HongyangWang QinghaiHuang TaoGuo ChenJi JianleiDong ZhenCao Yanwei - Vascular mural cells (VMCs) are crucial for vascular stability, and their dysfunction underlies cardiovascular pathologies including atherosclerosis and aortic aneurysms. PINCH proteins are core focal adhesion components mediating integrin signaling, yet their roles in VMC development remain elusive. Here, we generated mice with conditional deletion of both PINCH1 and PINCH2 in Pdgfrb-lineage VMCs, which resulted in perinatal lethality accompanied by severe arterial enlargement, hemorrhage and defective angiogenesis. Mutant VMCs exhibited profound defects in cytoskeletal organization, proliferation, differentiation, adhesion and extracellular matrix assembly. Multi-omics analyses revealed that PINCH deficiency dysregulated phospho-signaling networks, hyperactivating PDGFR/EGFR/AKT/ERK and STAT/NF-κB pathways while impairing integrin-FAK-SRC and cell cycle-associated pathways (p53, p27). RNA-seq demonstrated altered expression of genes enriched in immune response (CD74, Tlr2), cytoskeleton (TUBB3, ACTA2) and VMC differentiation (Rgs5, Kcnj8, ABCC9). Importantly, we identified PINCH1 as a nuclear transcriptional coregulator that directly represses proliferative-inflammatory programs while promoting contractile-adhesive and cytoskeletal organization signatures. The clinical relevance of these findings is underscored by downregulation of PINCH genes in human atherosclerosis and Marfan syndrome aneurysms, with conserved dysregulation of key PINCH targets including CD74 and RGS5. Our work reveals a dual cytoplasmic-nuclear mechanism for PINCH in maintaining vascular homeostasis, providing both mechanistic insights and therapeutic targets for vascular diseases. - Source: PubMed
Publication date: 2026/03/08
Wang ChunxiaoJin YaoXin YuanfengXing QiankeZhu HongmingZou QichengYan JieLuo LinaLiang XingqunSun YunfuLiu Zhongmin