ABCC3
- Known as:
- ABCC3
- Catalog number:
- 000909A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABCC3
Related genes to: ABCC3
- Gene:
- ABCC3 NIH gene
- Name:
- ATP binding cassette subfamily C member 3
- Previous symbol:
- -
- Synonyms:
- MRP3, cMOAT2, EST90757, MLP2, MOAT-D
- Chromosome:
- 17q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2018-05-03
Related products to: ABCC3
Related articles to: ABCC3
- The widespread application of glyphosate has resulted in the evolution of glyphosate resistance in Lolium rigidum. This study investigated the resistance mechanism in an Australian population of L. rigidum, designated WALR60. Transcriptome sequencing coupled with quantitative real-time PCR (qRT-PCR) analyses identified significant upregulation of ABCC3.2, ABCB11, and ABCC13 in the WALR60 population compared to susceptible controls. Structural analysis revealed that LrABCC3.2 lacks the N-terminal TMD0 domain present in its homolog LrABCC3.1, representing a core ABC transporter. LrABCC3.2-transformed yeast cells exhibited enhanced tolerance to glyphosate, as compared to the empty vector control. Similarly, rice calli and seedlings overexpressing ABCC3.2 (ABCC3.2-OE) showed increased glyphosate resistance relative to the corresponding GFP-overexpressing (GFP-OE) controls. Additionally, the LrABCC3.2-OE lines displayed resistance to haloxyfop and pinoxaden. Integrative transcriptomic and metabolomic analyses of transgenic rice revealed that LrABCC3.2 overexpression significantly enriches the glycerophospholipid metabolism pathway, with positive correlations between the expression of GPAT3, PLDα2, PLA14 and the accumulation of phosphatidylcholine (PC) and choline. Comparative transcriptome analysis between resistant L. rigidum and LrABCC3.2-OE rice identified 10 commonly upregulated and 18 commonly downregulated genes, indicating a conserved detoxification mechanism. In conclusion, this study demonstrates that ABCC3.2 overexpression contributes to glyphosate resistance in the WALR60 population and elucidates a potential downstream metabolic pathway involved in this trait. - Source: PubMed
Publication date: 2026/07/26
Ouyang YulanYing JinfengZeng YalinQi JialeLiu ZhanghuiPan Lang - The extensive use of Bacillus thuringiensis (Bt) insecticidal proteins in pest control has led to the evolution of resistance in target insects. Reduced toxin binding to the midgut epithelial membrane is considered a major resistance mechanism. Current methods for characterizing toxin binding suffer from limitations in physiological relevance or practical applicability. Here, we developed an in situ binding (ISB) method to visualize and quantify the binding of Cry1Ac toxin to the midgut epithelium of Helicoverpa armigera larvae. By culturing dissected midguts in a cell culture medium containing Cry1Ac, we maintained midgut cell viability over a short period while enabling specific toxin-receptor interactions under near-physiological conditions. Applying this method, we compared Cry1Ac binding to the midgut epithelium of a susceptible SCD strain and three SCD-derived Cry1Ac-resistant strains: SCD-r1 (deletion mutation in cadherin, conferring 438-fold recessive resistance), SCD-KI (T92C point mutation in tetraspanin, conferring 125-fold dominant resistance), and C2/3-KO (ABCC2 and ABCC3 knocked out, conferring >15,000-fold recessive resistance). All resistant strains exhibited significantly reduced Cry1Ac binding to the midgut epithelial membrane compared to the susceptible SCD strain, with 83.6%, 54.4%, and 31.7% decreases in Cry1Ac signal fluorescence intensities in the C2/3-KO, SCD-KI, and SCD-r1 strains, respectively. Moreover, the reduction in Cry1Ac binding correlated with a marked decrease in toxin-induced midgut epithelial damage in the resistant strains. Our findings provide additional evidence for reduced toxin binding as a shared mechanism of Cry1Ac resistance in H. armigera across diverse genetic basis. The established ISB method provides a valuable tool for evaluating the binding of Bt toxins and other insecticidal proteins to the insect midgut epithelium. - Source: PubMed
Publication date: 2026/07/21
Sun QimingGuan FangShen HuiwenLi KaixiaYang YihuaHe Ya-ZhouWu Yidong - Bile acids (BAs) are steroidal molecules with endocrine and exocrine functions, eliminated primarily via bile. Intrahepatic cholestasis of pregnancy (ICP) features elevated maternal BA concentrations linked to adverse perinatal outcomes. Hypertensive disorders of pregnancy, often managed with methyldopa, co-occur with BA dysregulation, yet the impact of methyldopa on BA homeostasis is unclear. We examined methyldopa in a murine model of estrogen-induced cholestasis. Female C57BL/6J mice received ethinylestradiol (10 mg/kg, s.c.) with or without methyldopa (250 mg/kg, p.o.) for 7 days. BA profiles were quantified by LC-MS across plasma, bile, liver, urine, intestine, and feces. Hepatic, ileal, and renal expression of BA-related enzymes/transporters was assessed by RT-qPCR and Western blotting. In estrogen-challenged mice, methyldopa selectively reduced total BA concentrations in plasma and liver without increasing fecal or urinary BA excretion. The lowering coincided with induction of CAR-responsive detoxification/export markers, particularly Cyp2b10 and Abcc3/Mrp3, together with partial restoration of nuclear CAR and reduced p-ERK1/2 normalized to total ERK1/2. Methyldopa also reduced hepatic free cholesterol in cholestatic mice, accompanied by reduced Hmgcr abundance and increased Acat2 expression, indicating altered cholesterol handling that may limit substrate availability for BA synthesis. In conclusion, methyldopa lowered BA plasma concentrations under estrogenic stress consistent with reduced substrate availability for BA synthesis and enhanced detoxification/export. In the context of pregnancy-related BA dysregulation, these findings suggest that methyldopa, when used for hypertensive disorders of pregnancy, does not exacerbate BA accumulation and may selectively attenuate it; this hypothesis warrants clinical evaluation. - Source: PubMed
Publication date: 2026/08/25
Manna Dina FLastuvkova HanaSchreiberova JolanaJandova LenkaHroch MilosAmbroz MartinBajnokova MariaLenicek MartinHirsova PetraKacerovsky MarianNekvindova JanaPavek PetrMicuda Stanislav - The yellowfin seabream (Acanthopagrus latus) is a significant economic fish along the southeast coast of China. Recently, the drastic decline in the wild populations, exacerbated by overfishing and climate change, has heightened our reliance on aquaculture. However, the current lack of research on its domestication hinders effective conservation of wild populations and balanced management alongside the aquaculture industry. Studies on body characteristics have shown that wild yellowfin seabream possess a higher body, while cultured ones exhibit a wider body. Whole-genome SNP analysis revealed moderate genetic differentiation between cultured and wild populations. Further analyses of linkage disequilibrium, heterozygosity, and genetic diversity revealed that the degree of SNP linkage was lower in the wild population compared to the cultured population. In contrast, heterozygosity and nucleotide polymorphisms were significantly higher in the wild population (P < 0.001 and P < 0.05, respectively). Additionally, over 300 candidate genes were identified in each cultured population through genomic selection signature analysis, with 67 key genes shared among all three, which were linked to growth and development (ghrb, ghsra, and cfl1), immune response (aire, cd36, and igbp1), and salinity adaptation (abcc3, clic4, and kcnk15). Enrichment analysis indicated that the key candidate genes were significantly enriched in pathways related to protein kinase activity, ion binding and growth hormone synthesis, secretion and action (FDR < 0.05). The findings provide valuable insights into the variation in body size of yellowfin seabream under domestication selection and offer an important theoretical basis for the genetic improvement of yellowfin seabream. - Source: PubMed
Publication date: 2026/08/13
Gao ZhanyuanWang WenhaoLiang XuanguangHuang JunrouHu YanFeng JianxiangLu Jianguo - Hantavirus infection triggers life-threatening hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS), driven by severe endothelial barrier breakdown and systemic capillary leakage. Clinical severity varies widely with undefined host regulators, and no targeted endothelial-protective treatments exist. Recent data link hantaviruses to gut microbiome remodeling, while bile acid (BA) receptors FXR and TGR5 potently inhibit NF-κB-mediated endothelial inflammation. We synthesize four core lines of evidence. First, metagenomic reports confirm hantavirus reshapes gut/lung microbiota in rodent reservoirs. Second, we re-analyzed three public GEO datasets via standardized RNA-seq/microarray pipelines: (i) GSE245916: SEOV-infected human/rat lung ECs show conserved VCAM1/ICAM1 upregulation (human VCAM1 logFC=+1.17, P = 0.023; rat Icam1 logFC=+0.32, padj=0.016) with unaltered FXR; (ii) GSE7271: SEOV-infected rat lung displays sustained Nfkb1 suppression (all timepoints, P<0.05) and day-15 Slc10a2 downregulation (P = 0.028); (iii) GSE270172: PUUV 3D vessel chips feature robust IL6 elevation (logFC=+1.22, P = 3.1×10) and disrupted BA transporters (ABCC3 logFC=-1.44, P = 7.4×10¹²). TGR5 (GPBAR1) was undetectable in endothelial cells across all datasets. Third, FXR/TGR5 agonists repress NF-κB inflammation and mitigate lung vascular injury. Fourth, HTNV upregulates CH25H to block HMGCR-dependent cholesterol synthesis, depleting BA precursor substrates. We propose a unified pathogenic model: hantavirus-triggered gut dysbiosis plus virus-impaired cholesterol metabolism deplete circulating FXR/TGR5 agonistic BAs, relieving constitutive inhibition of endothelial NF-κB and monocyte NLRP3 inflammasomes to exacerbate capillary leakage. We define tiered testable predictions covering clinical multi-omics cohorts, receptor modulation assays and pharmacological interventions. This gut microbiota-BA-FXR/TGR5 axis represents a repurposable therapeutic target for hantavirus diseases, though direct causal evidence connecting BA signaling to viral vascular damage remains absent; our framework offers a rigorous testable roadmap for subsequent validation. - Source: PubMed
Publication date: 2026/07/22
Liu LeiLin JiyongSang KaiLai JianpingHuang NaZhong PeilingLiu YuxiangChen Sheng