Ask about this productRelated genes to: ACIN1 antibody
- Gene:
- ACIN1 NIH gene
- Name:
- apoptotic chromatin condensation inducer 1
- Previous symbol:
- ACINUS
- Synonyms:
- KIAA0670, fSAP152
- Chromosome:
- 14q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-14
- Date modifiied:
- 2014-11-18
Related products to: ACIN1 antibody
Related articles to: ACIN1 antibody
- Rhotekin (RTKN), a Rho GTPase effector, promotes the development of malignancies, including breast, gastric, and colon cancers, by enhancing cell proliferation and migration while inhibiting apoptosis. Despite its oncogenic role, the phosphoregulatory network of RTKN remains largely unexplored, with no experimental evidence on its upstream kinases and functional phosphosites. To characterize RTKN-associated phosphorylation dynamics, PubMed-indexed studies were systematically retrieved using predefined MeSH terms to compile large-scale cellular phosphoproteomics datasets. Analysis of 618 quantitative profiling and 179 differential abundance datasets identified 27 Class-I phosphosites in RTKN. Among these, five sites-Ser106, Ser220, Ser520, Ser529, and Ser543 were consistently observed across multiple datasets, suggesting them as predominant sites with potential functional significance. Structural mapping of predominant sites onto the AlphaFold2-predicted model indicated that these sites are located in accessible regions, highlighting their potential susceptibility to kinase-mediated regulation. As these sites represent understudied phosphosites, a robust strategy was employed to identify their functional role by assessing co-regulated phosphosites on other proteins (PsOPs). ACIN1_Ser243, CTNNA1_Ser641, and SHROOM2_Ser1036 were among the top positively co-regulated PsOPs, whereas MICALL1_Ser644, PRP4K_Ser366, and MYO18A_Ser1970 were negatively co-regulated. PsOPs were mainly involved in apoptosis, cell growth, motility, and cytoskeletal reorganization, suggesting potential functional convergence with RTKN. Additionally, phosphorylation at RTKN Ser520 and Ser543 co-occurred across multiple datasets. Moreover, TRPM7 and PAK4 were identified as predicted upstream kinases phosphorylating RTKN at Ser220 and Ser520. Pathway analysis showed involvement of co-regulated proteins in cancer-associated signaling pathways. These findings provide a foundation for future research to elucidate the phosphosite-specific role of RTKN in cancer. - Source: PubMed
Publication date: 2026/04/10
Palollathil AkhinaMahin AlthafGopalakrishnan Athira PerunellySambreena AlimathUmmar SamseeraShivamurthy Prathik BasthikoppaGanesan RVijayakumar ManavalanRaju Rajesh - Eukaryotic pathogens deploy diverse strategies to manipulate host immunity, yet RNA-based virulence mechanisms remain poorly understood. We describe a mechanism by which the malaria parasite Plasmodiumfalciparum governs host immune responses through direct interference with host nuclear RNA processing. Malaria-encoded mRNAs of the early transcribed membrane protein family, exported from infected red blood cells, evade cytoplasmic degradation within host immune cells and are imported into their highly secured nuclei. Inside the nucleus, parasite transcripts bind the host RNA-binding proteins ACIN1 and PNN, key components of the splicing machinery that associate with the exon junction complex. This interaction disrupts host splicing regulation, leading to widespread misprocessing of transcripts and altered expression of proteins involved in immune function. Our findings uncover an RNA-based strategy by which pathogen-derived transcripts exploit the host splicing machinery, reshaping transcript isoform landscapes and immune signaling. - Source: PubMed
Publication date: 2026/02/13
Abou Karam PaulaKiper EdoZiv TamarYadid ShakedKozela EwaZharoni NirNevo ReinatAlfandari DanielOtesh HelinaCruz Camacho AbelLubelsky YoavRotkopf RonWeizman EviatarCossin MosheRosenhek-Goldian IritPetrovich-Kopitman EkaterinaPorat ZivShoshani OferUlitsky IgorLevy CarmitMelamed ZeevRegev-Rudzki Neta - Extensive-stage small-cell lung cancer (ES-SCLC) is associated with a poor prognosis. Although first-line immunochemotherapy improves clinical outcomes, robust prognostic biomarkers for this treatment modality remain unavailable. The aim of this study was to identify non-invasive, easily accessible, and dynamically monitored biomarkers of ES-SCLC by machine learning integrating serum metabolomics, lipidomics, and proteomics at multiple time points. - Source: PubMed
Publication date: 2026/02/07
Zheng LiangXu HaomingWang ShuyuanMa MeiliHu FangCheng LeiLu JunPan FengZhang BoXu JianlinLi YingShen YinchenZhang WeiZhong RunboChu TianqingHan BaohuiZheng XiaoxuanZhong HuaNie WeiZhang Xueyan - Nonalcoholic fatty liver disease (NAFLD), which affects approximately 25% of the adult population, represents a significant contributor to liver-related morbidity and mortality. However, the molecular mechanisms underlying NAFLD-related liver fibrosis remain incompletely understood. Moreover, there is a lack of research integrating transcriptomic data with MRI-derived parameters. - Source: PubMed
Publication date: 2025/11/15
Liang YaoHu NaXia XingLi FangyanYang MeihuaLei PingguiLuo Peng - NUTM1-rearranged (NUTM1-R) infant acute lymphoblastic leukaemia (ALL) is a newly identified subgroup of non-KMT2A-R infant ALL, with ACIN1::NUTM1 the most frequent fusion. KMT2A-R and NUTM1-R infant ALL are characterized by fewer copy number alterations. Moreover, the gene expression profile in NUTM1-R infant ALL characteristically reveals upregulation of the genes that are involved in KMT2A-R infant ALL development, including HOXA9 and HOXA10. However, the direct association of NUTM1-fusion with this gene expression remains unexplored. Clinically, in sharp contrast to KMT2A-R infant ALL, the prognosis of NUTM1-R infant ALL is excellent, although its drug sensitivity profile remains unclear. Here, we newly identified an ACIN1::NUTM1-positive ALL cell line, KOPN32, which was previously established from a relapsed infant-ALL case, as the only cell line with NUTM1-fusion. KOPN32 had fewer copy number alterations, like KMT2A-R ALL cell lines. Both KOPN32 and an ACIN1::NUTM1-inducible ALL model, which was established using the ACIN1::NUTM1 fusion cDNA subcloned from KOPN32, revealed upregulation of HOXA9, HOXA10, SKIDA1 and BMI1, indicating direct involvement of ACIN1::NUTM1 fusion in the upregulation of these genes. In the drug sensitivity to eight standard agents, KOPN32 showed high sensitivity to both daunorubicin and vincristine; both are crucial agents in the induction therapy for infant ALL. - Source: PubMed
Publication date: 2025/08/29
Tamai MinoriKomatsu ChiakiKagami KeikoKasai ShinWatanabe AtsushiAkahane KoshiGoi KumikoTomoyasu ChihiroImamura ToshihikoOguri SatoshiIwasaki SumioTeshima TakanoriYatabe YasushiInukai Takeshi