ANLN
- Known as:
- ANLN
- Catalog number:
- 001666A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ANLN
Related genes to: ANLN
- Gene:
- ANLN NIH gene
- Name:
- anillin actin binding protein
- Previous symbol:
- -
- Synonyms:
- ANILLIN, Scraps, scra
- Chromosome:
- 7p14.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-03
- Date modifiied:
- 2016-10-05
Related products to: ANLN
Related articles to: ANLN
- Prostate cancer (PCa) and Alzheimer's disease (AD) are age-related disorders with a complex epidemiological association and limited therapeutic options. Identifying shared molecular drivers may reveal new treatment targets. - Source: PubMed
Publication date: 2026/08/20
Wang MengxueQian YanrongHuang EnyaoChu ChunyanGao TianChen ShengrongZhao NaLuo CaichenLiu YifanZheng XiejunhaoHu HaowenHan BowenChen MingMao WeipuLi Wenchao - Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies worldwide, characterized by late diagnosis, rapid progression and resistance to conventional therapies. Cancer‑associated fibroblast (CAF)‑derived extracellular vesicles (EVs) contribute to PDAC progression, but their downstream molecular effectors remain unclear. In the present study, it was demonstrated that CAF‑derived EVs enhanced the proliferative, migratory and invasive capacity of PDAC cells across two independent cell lines, as assessed by Cell Counting Kit‑8 assays and Transwell migration and Matrigel invasion assays. RAP1B was identified as a prominently upregulated protein by label‑free proteomic profiling following EV exposure. High RAP1B expression, evaluated by immunohistochemistry, in a cohort of 77 resected PDAC specimens tended to be more frequent with advancing pathological stage and was associated with poorer overall survival. RAP1B knockdown using small interfering RNA suppressed proliferation and motility in PDAC cells and induced cytokinesis failure characterized by multinucleation and cytoskeletal abnormalities, as demonstrated by time‑lapse imaging and immunofluorescence staining. Proteomic profiling of RAP1B‑knockdown cells identified anillin (ANLN) as a downstream mediator; ANLN knockdown recapitulated these cytokinetic defects, whereas ANLN knockdown did not reciprocally affect RAP1B levels, establishing a unidirectional RAP1B/ANLN axis. Furthermore, RAP1B depletion sensitized PDAC cells to gemcitabine, showing additive growth inhibition. In conclusion, CAF‑derived EVs mediate PDAC progression via the RAP1B/ANLN axis, representing a novel and promising therapeutic target in PDAC. - Source: PubMed
Publication date: 2026/08/21
Yoshimori DaigoKudo MitsuhiroIshino KousukeUeda JunjiShintani-Domoto YukakoMatsushita AkiraKawano YouichiOno TakashiHaruna TakahiroEndo KazuhikoHamaguchi AkiraFujii TakenoriKawamoto YokoTeduka KiyoshiKitamura TaekoMasamune AtsushiMatsuda AkihisaYoshida HiroshiOhashi Ryuji - Lung adenocarcinoma (LUAD) has a poor prognosis, and effective metabolic biomarkers are still few. Glutamine metabolism is one of the central features of tumor metabolic reprogramming, but the cellular heterogeneity and clinical significance of glutamine metabolism in the LUAD tumor microenvironment (TME) remain unknown. The goal of this paper was to define glutamine metabolism on a single-cell basis and determine major regulators that have predictive value. - Source: PubMed
Publication date: 2026/07/16
Ma YimingZhang ZhihanPan HongliJiang HailinGuo LiliGuo Fengjie - Insect wing polyphenism enables a single genome to produce distinct wing morphs in response to environmental cues, yet its underlying cellular determinants remain elusive. Here, we perform single-cell RNA sequencing of long-winged- and short-winged-destined wing buds of Pyrrhocoris apterus and Nilaparvata lugens, identifying six conserved cell types with comparable proportions between the two morphs. RNA interference-mediated silencing of 51 marker genes indicates that wing-patterning genes En (epithelial-like cells) and bs (tracheal cells), and cell-cycle genes Anln, CycB3, and cdk1 (neuron cells), are essential for long-winged development, among which En exhibits a specific temporal requirement. Flow cytometry analysis shows that long-winged formation mainly relies on an extended duration of cell proliferation. Cross-species comparisons indicate shared wing cell identities. Our findings indicate that hemipteran short-winged morphs may evolve from ancestral long-winged forms via precise regulation of wing-patterning and cell-cycle gene expression in epithelial‑like, tracheal, and neuron cells. This provides insights into the developmental plasticity of insect tissues at single‑cell resolution. - Source: PubMed
Publication date: 2026/07/02
Wan YiWu Hui-JieHuang Heng-GuangLiu Zhuo-QiSun Zhao-XiangYang Zhang-NvXu Hai-Jun - Adult human hearts show limited regeneration after acute myocardial infarction (AMI) despite a small subpopulation (~5%) of cardiomyocytes re-entering the cell cycle. We integrated public single-nucleus RNA-seq, spatial transcriptomics, bulk RNA-seq and ATAC-seq datasets from human fetal hearts and adult infarcted hearts to investigate why cell-cycle-active cardiomyocytes fail to complete division. These cells were enriched in the infarct zone (IZ) and activated early cell-cycle programs, but showed insufficient reactivation of late mitotic and cytokinesis execution machinery, particularly ANLN and KIF18A, and instead engaged stress-adaptive programs. Multi-omics filtering across expression, chromatin accessibility, and co-expression/regulatory networks highlighted five developmental cell-cycle-associated genes with insufficient adult reactivation: ANLN, KIF18A, MDK, RTKN2, and SOX11. In human induced pluripotent stem cell-derived cardiomyocytes, hypoxia suppressed most candidates, whereas MDK retained responsiveness to pro-proliferative Wnt stimulation. These findings suggest that incomplete cytokinesis reactivation represents a key bottleneck for adult human cardiac regeneration, and nominate MDK as a tractable candidate for chemical biology and drug-discovery efforts aimed at promoting cardiomyocyte cell-cycle completion. - Source: PubMed
Lyu JieranKuramoto YukiLi JunLee Jong-KookHidaka KyokoSakata Yasushi