ABLIM3
- Known as:
- ABLIM3
- Catalog number:
- 000962A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABLIM3
Related genes to: ABLIM3
- Gene:
- ABLIM3 NIH gene
- Name:
- actin binding LIM protein family member 3
- Previous symbol:
- -
- Synonyms:
- KIAA0843
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-22
- Date modifiied:
- 2019-03-21
Related products to: ABLIM3
Related articles to: ABLIM3
- African zebu cattle (Bos indicus) exhibit remarkable adaptations to extreme thermal conditions, yet the genomic basis of this resilience remains incompletely characterized. Ethiopia provides a unique natural setting in which closely related zebu populations have adapted divergently to dry-hot (DHETZ) and humid-hot (HHETZ) climates. In this study, we reanalyzed publicly available whole-genome sequencing datasets from 46 Ethiopian zebu cattle from five populations and compared them with Asian zebu, Sudanese zebu, African taurine, and European taurine breeds. By integrating genome-wide SNP analysis, population genetic structure assessment, and multiple selection scans (iHS, Hp, XP-EHH, and XP-CLR), we identified distinct and shared selection signatures between DHETZ and HHETZ. We detected 33.7 million and 34.2 million biallelic autosomal SNPs in DHETZ and HHETZ, respectively. Ethiopian zebu clustered closely with Sudanese zebu but showed clear divergence from Asian zebu and taurine breeds. DHETZ and HHETZ exhibited very low genetic differentiation (FST = 0.0063), consistent with their shared ancestry; however, each group displayed unique selection signals. In DHETZ, iHS and Hp detected 298 and 113 candidate regions, respectively, whereas in HHETZ, they detected 244 and 138 regions, respectively. Cross-population XP-EHH and XP-CLR analyses identified 163 and 227 divergent regions between DHETZ and HHETZ, respectively. Integration of the four selection scans identified 19 high-confidence candidate regions in DHETZ and 13 in HHETZ. DHETZ showed strong selection in genes involved in oxidative stress regulation, protein folding, mitochondrial function, and vascular remodeling, including SESN2, DNAJC8, GRPEL2, ABLIM3, and AFAP1L1. In contrast, HHETZ displayed signatures in genes associated with immune responses, energy metabolism, and angiogenesis inhibition, including MYD88, PRKACA, PRKACB, and WIF1. Several genes, including VEGFC, TNIP3, and DMXL2, were under selection in both groups, suggesting conserved mechanisms of thermotolerance and reproductive adaptation. The shared VEGFC signal and the HHETZ-specific WIF1 signal may indicate a distinct vascular regulatory mechanism in the dry-hot and humid-hot environments. Our results reveal a dual pattern of genomic adaptation in Ethiopian zebu cattle and provide candidate loci for future validation and climate-resilient livestock breeding. - Source: PubMed
Publication date: 2026/09/03
Terefe EndashawBelay GurjaTijjani AbdulfataiBarbosa da Silva Marcos ViniciusHan JianlinSalim BashirHanotte Olivier - Gene-level analysis of RNA-Seq data provides only a partial view of muscle transcriptional regulation because gene isoforms may be differentially used without changes in total gene expression. This study evaluated the extent and potential role of differential transcript usage (DTU) during breast muscle development from the late embryonic stage to market age. Publicly available RNA-Seq data from breast muscle of Cornish, White Plymouth Rock, and their crossbred progeny sampled at embryonic day 17 (ED17) and post-hatch days 1, 21, and 42 were analyzed using The R package IsoformSwitchAnalyzeR (n = 6 samples per genetic background and stage, total = 72 samples). The highest number of isoform switches (|Δ isoform fraction| > 0.1 and FDR < 0.05) occurred during ED17-to-D1 transition (933 switches), followed by D1-to-D21 (631 switches), whereas only 46 occurred between D21 and D42. Exon skipping, alternative transcription start sites, and alternative transcription termination sites were the most frequent splicing events associated with these switches (n = 1,042, 964, and 817, respectively). Changes in coding sequence completeness, intrinsically disordered regions, and protein domains were the most frequently predicted functional consequences (n = 497, 472, and 461 events, respectively). Gene ontology enrichment (P < 0.05) indicated that ED17-to-D1 switching genes were involved in sarcomeric and cytoskeletal organization, redox and metabolic adaptation, signaling, chromatin regulation, and RNA processing, with top genes including OBSCN, DTNA, ABLIM3, and LIMCH1. D1-to-D21 switching genes were associated with cytoskeletal restructuring, adhesion and mechanosensing, RNA processing, protein turnover, autophagy, metabolic adaptation, and stress signaling, with TNNT3, FHL1, and FHL3 among the top-ranked genes. Although fewer genes exhibited isoform switching during the D21-to-D42 transition, the top-ranked genes included MYH1B, SMYD1, and MRTFA, which are involved in contractile or muscle regulatory processes. In conclusion, isoform switching represents an additional layer of transcriptional regulation of muscle development and it may contribute to hatch-related maturation, rapid post-hatch growth, and later refinement of contractile function. Future studies should experimentally validate candidate switches and their predicted functional consequences. - Source: PubMed
Publication date: 2026/08/05
Alnahhas Nabeel - Epidermal growth factor receptor-targeted therapies such as afatinib provide clinical benefits to patients with advanced-stage non-small cell lung cancer (NSCLC); however, acquired resistance frequently develops, with the underlying mechanisms remaining undefined in 20-30% of cases. The present study established afatinib-resistant (AR) NSCLC cell lines and confirmed their resistance phenotype using Cell Counting Kit-8 (CCK-8) cell viability assays. Notably, these cells also exhibited cross-resistance to osimertinib. To elucidate the molecular basis of resistance acquisition, the time-resolved transcriptomic profiling of A549 cells was performed across three stages: Parental, afatinib-exposed (adaptive phase) and stable resistant cells. The analyzed results revealed the persistent upregulation of and , which was validated by reverse transcription-quantitative polymerase chain reaction. The meta-analysis of hazard ratios from The Cancer Genome Atlas demonstrated that the elevated expression level of the three-gene signature was significantly associated with tumor progression and an increased risk of disease recurrence. These transcriptional alterations were accompanied by the sustained activation of the MAPK/ERK signaling pathway, as evidenced by increased ERK1/2 phosphorylation detected using western blot analysis, which was positively associated with the expression level of the three-gene signature. Functional analyses further demonstrated that the pharmacological inhibition of MAPK/ERK signaling using selumetinib effectively re-sensitized AR cells to both afatinib and osimertinib, as demonstrated by restored drug sensitivity in CCK-8 assays. Collectively, these findings suggest that MAPK/ERK signaling contributes to the transition from adaptive tolerance to stable resistance to afatinib and highlight a tractable therapeutic vulnerability for overcoming resistance to tyrosine kinase inhibitors in NSCLC. - Source: PubMed
Publication date: 2026/07/17
Qin ChangtaiZhang WeiTang DongfangYang YuxiLiang BinghuiHu ZhimingZhang YuxiaoYe TingjieXu Wei - The Tumour Protein D52 (TPD52) family, including TPD52, TPD52L1, and TPD52L2, plays critical roles in membrane trafficking, lipid metabolism, and oncogenic signalling, with its overexpression linked to multiple cancers. Phosphorylation is a key regulator of their functions, yet their phosphoproteomic landscape remains underexplored. This study integrates over 3,825 public human phosphoproteomic datasets to map phosphorylation profiles of TPD52, TPD52L1, and TPD52L2, identifying dominant phosphosites like S171, S176, S149, and S12, S166 within conserved coiled-coil and PEST-like domains. CAMK2D was identified as a predominant shared kinase, alongside CDK2 and GRK5, associating these modifications with calcium signaling, cell cycle progression, and cytoskeletal remodeling. Co-phosphoregulation highlighted positive interactions with ABRAXAS2 and negative correlations with ABLIM3, implicating involvement in ubiquitin-mediated degradation, epithelial-mesenchymal transition (EMT), and cytokinesis. Notably, hypophosphorylation at TPD52_S171/S176 was observed in hepatocellular and lung carcinomas, whereas hyperphosphorylation at TPD52L2_S166 prevailed in ovarian and pancreatic cancers, underscoring biomarker utility. Phosphorylation-driven interactomes emphasized roles in vesicular trafficking and oncogenesis This study catalogues the phosphorylation events and explores the potential of TPD52 family as a phosphoregulated hub in cancer biology, with CAMK2D as a potential therapeutic target. - Source: PubMed
Publication date: 2025/12/09
Khan Noreen AFahma AmalMahin AlthafGopalakrishnan Athira PerunellyShivamurthy Prathik BasthikoppaRajeev Athira CRaju Rajesh - [This corrects the article DOI: 10.1016/j.csbj.2024.04.024.]. - Source: PubMed
Publication date: 2024/10/26
Gong BaochengQu TongyuanZhang JiaojiaoJia YubinSong ZianChen ChongYang JiaxingWang ChaoyuLiu YunJin YanCao WenfengZhao Qiang