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
- 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 - Lung adenocarcinoma (LUAD) is one of the most common malignant tumors. Although several treatments have been proposed, the long-term prognosis of this cancer is poor. Lipid droplets and mitochondria are important organelles that regulate energy metabolism in cells and are postulated to promote the occurrence and progression of tumors. However, few risk prediction models have been constructed based on lipid drop-mitochondria-related genes (LMRGs). - Source: PubMed
Publication date: 2024/11/17
Cai RuijuanLin HongshengCheng QianwenMao QiyuanZhang ChuchuTan Ying - Oesophageal cancer (EC) is a malignancy which accounts for a substantial number of cancer-related deaths worldwide. The molecular mechanisms underlying the pathogenesis of EC have not been fully elucidated. GSE17351 and GSE20347 data sets from the Gene Expression Omnibus (GEO) database were employed to screen differentially expressed genes (DEGs). Reverse transcription quantitative PCR (RT-qPCR) was used to examine hub gene expression. ECA-109 and TE-12 cells were transfected using the pcDNA3.1 expression vector encoding GABRP. The cell counting kit-8 (CCK-8), cell scratch and Transwell assays were performed to assess the effect of GABRP on EC cell proliferation, migration and invasion. Epithelial-mesenchymal transition (EMT)-associated protein levels were measured by Western blotting. Subsequently, CFTR was knocked down to verify whether GABRP affected biological events in EC cells by targeting CFTR. Seven hub genes were identified, including GABRP, FLG, ENAH, KLF4, CD24, ABLIM3 and ABLIM1, which all could be used as diagnostic biomarkers for EC. The RT-qPCR results indicated that the expression levels of GABRP, FLG, KLF4, CD24, ABLIM3 and ABLIM1 were downregulated, whereas the expression level of ENAH was upregulated. In vitro functional assays demonstrated that GABRP overexpression suppressed the proliferation, migration, invasion and EMT of EC cells. Mechanistically, GABRP promoted the expression of CFTR, and CFTR knockdown significantly counteracted the influence of GABRP overexpression on biological events in EC cells. Overexpression of GABRP inhibited EC progression by increasing CFTR expression, which might be a new target for EC treatment. - Source: PubMed
Publication date: 2024/07/11
Zhang JingzhiLiu XueZeng LingHu Ying