Ccnl1 antibody - N-terminal region (ARP33175_P050)
- Known as:
- Ccnl1 (anti-) - N-terminal region (ARP33175_P050)
- Catalog number:
- arp33175_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Ccnl1 antibody - N-terminal region (ARP33175_P050)
Related genes to: Ccnl1 antibody - N-terminal region (ARP33175_P050)
- Gene:
- CCNL1 NIH gene
- Name:
- cyclin L1
- Previous symbol:
- -
- Synonyms:
- ania-6a
- Chromosome:
- 3q25.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-03-07
- Date modifiied:
- 2015-08-24
Related products to: Ccnl1 antibody - N-terminal region (ARP33175_P050)
Related articles to: Ccnl1 antibody - N-terminal region (ARP33175_P050)
- Understanding regulatory interactions between hepatitis B virus (HBV) and host factors is essential for the development of next generation host-directed antiviral therapies and the achievement of a functional HBV cure. Here, we investigated HBV-induced alterations in host gene expression in primary human hepatocytes (PHH) to identify host factors exploited by the virus for replication and persistence. Whole-transcriptome sequencing (WTS) of HBV-infected PHH identified host pathways with potential roles in the HBV life cycle. RNA interference-based functional screening of dysregulated candidate genes identified cyclin L1 (CCNL1) as a key host factor. RNAi-mediated knockdown of CCNL1 reduced HBV gene expression, including hepatitis B surface antigen (HBsAg). Mechanistically, CCNL1 regulates phosphorylation of the C-terminal domain (CTD) of RNA polymerase II (RNAPII) at serine 2 (S2), consistent with a role in transcriptional regulation. CCNL1 knockdown further reduced the binding of total and phospho- (Ser2/Ser5) RNAPII, pan-acetylated histone H3 (H3ac), and H3K27ac to HBV covalently closed circular DNA (cccDNA), indicating impaired cccDNA-dependent transcription. In addition, CCNL1 expression was elevated in chronic hepatitis B patients compared with those with resolved infection. Collectively, these data demonstrate that CCNL1 promotes HBV transcription and replication through modulation of RNAPII phosphorylation and chromatin-associated transcriptional activity, identifying CCNL1 as a potential host susceptibility factor for HBV. - Source: PubMed
Publication date: 2026/05/08
Owino Collins OduorNarmada Balakrishnan ChakrapaniYi Lin GianAw Pauline Poh KimGanesh NivrithiSiying Jovi TanPlissonnier Marie-LaureMatan Thangavelu ThangaveluShirgaonkar NiranjanBifani PabloLevrero MassimoPeriyasamy GiridharanGee Lim SengDasGupta Ramanuj - Current clinical tools for predicting relapse and guiding adjuvant therapy in clear cell renal cell carcinoma (ccRCC) lack precision, especially in intermediate-risk disease. This study evaluated whether a nonproliferative tumor cell phenotype, P21 (CDKN1A inhibitor)-positive and MCM2 (DNA replication protein)-negative (P21+/MCM2-), could serve as a robust biomarker to improve prognostic stratification and guide postnephrectomy treatment decisions. We used multiplex immunofluorescence and Artificial Intelligence-based image analysis on nephrectomy specimens from three independent ccRCC cohorts: UK arm of the SORCE trial (n = 382), Korean (n = 71), and Scottish (n = 88). An optimal 2% cutoff for P21+/MCM2- cells was determined using X-tile software. Additional analyses assessed endoglin/CD105 coexpression, paired primary-metastatic samples (n = 41), and associations with adjuvant sorafenib therapy. In two intermediate-risk ccRCC cohorts (SORCE, n = 63; Korean, n = 71), patients with >2% P21+/MCM2- cells had significantly longer time to relapse [HR = 0.17; 95% confidence interval (CI), 0.06-0.54; HR = 0.27; 95% CI, 0.10-0.72]. Prognostic value was confirmed in high-risk (SORCE, HR = 0.43; 95% CI, 0.19-0.99) and all-risk (Scottish, HR = 0.37; 95% CI, 0.14-0.98) cohorts. Notably, patients with high P21+/MCM2- levels on placebo fared better than those receiving adjuvant TKI therapy (HR = 0.29; 95% CI, 0.16-0.50). In 41 paired samples, 85% showed higher P21+/MCM2- abundance in metastases than in primary tumors. As a conclusion, P21+/MCM2- cell count is a robust biomarker that refines relapse risk stratification in ccRCC and identifies patients who may not benefit from adjuvant tyrosine kinase inhibitor (TKI) therapy. High levels of these nonproliferative, senescent-like cells suggest tumor dormancy and a more favorable outcome without treatment. - Source: PubMed
Abdullah HazemUm In HwaStewart Grant DJeong Chang WookKwak CheolMoon Kyung ChulLaird AlexanderFrangou ElenaEisen TimMeade AngelaHarrison David J - Pooled analysis of the SPOTLIGHT and GLOW phase III trials, involving 1072 patients with locally advanced or metastatic gastric/gastroesophageal junction (GC/GEJ) adenocarcinoma positive for claudin18.2 (CLDN18.2) and negative for HER2, showed that zolbetuximab combined with chemotherapy significantly improved progression-free survival (PFS) compared to placebo (HR = 0.72; 95% CI, 0.61-0.84). Subgroup analyses revealed better outcomes in Asian patients, those with gastric cancer, and those with intestinal-type GC. In a cohort of 92 GC patients (immunohistochemical detection based on a CLDN18.2 subtype-specific antibody), CLDN18.2 positivity was associated with lymph node metastasis, advanced cancer stages (III-IV), and shorter overall survival (OS) (HR = 1.728; 95% CI, 1.003-2.977; P = 0.0404). In our study, knockdown of CLDN18.2 inhibited tumor growth in vivo and in vitro. Additionally, CLDN18.2 knockdown down-regulated minichromosome maintenance (MCM) proteins, particularly MCM2 and MCM5, and decreased phosphorylation of ERK, CDK, and MCM2 in GC cells. These findings provide a theoretical basis for the future selection of advantageous populations for CLDN18.2-targeted therapy and combination therapy strategies. - Source: PubMed
Publication date: 2026/02/23
Zheng BowenFu MiaoLou FanzhuoranHe YutingZhao LingyingHuang XintianXie XiaowenTan WeijuanChen QuanZhang WenqingHong YongxiangRong KaiyiLu YuyanZhan PingTu JingkeShi HuiboHu TianhuiXiao Li - Chromatin loading of the hexameric replicative helicase MCM2-7 complex requires coordinated interactions with the origin recognition complex (ORC), CDC6, and CDT1. MCM2-7 not bound to DNA forms a single hexamer (SH) with an open DNA entry gate between MCM2 and MCM5. Two MCM2-7 SHs can be loaded sequentially to form the double hexamer (DH) that encircles the DNA duplex. Activated MCM2-7 then unwinds DNA and initiates DNA replication. Our cryoelectron microscopy analyses show that a fraction of human MCM2-7 without DNA exists as DH. Unexpectedly, we find that the MCM3 winged helix domain (WHD) docks on MCM2 in both DNA-free DH and SH, creating a safety latch across the DNA entry gate to block DNA entry into the central channel. The safety latch can be opened by ORC-CDC6 binding. Perturbing this latch by structure-based or disease-related mutations of MCM3 causes replication defects and DNA damage checkpoint activation. Shortening the MCM3 linker between the helicase domain and WHD alleviates the cell cycle defects of the latch-strengthening mutation. Our findings uncover a regulated step in MCM2-7 loading with implications for human diseases. - Source: PubMed
Publication date: 2026/02/20
Liu YusongYang MengquanLu PingGao HaishanHe MaozhouWang YitaoQi AoCao TingZhang QiuqinQi ShutaoShi YigongYu Hongtao - Cyclin L1 (CCNL1) is highly expressed in multiple cancer types and has been linked to poor prognosis. However, the expression pattern of CCNL1 in breast cancer and its specific role in regulating breast cancer progression remain largely unknown. This study used cell and molecular biology techniques to examine how CCNL1 regulates the proliferation, invasion, migration, and epithelial-mesenchymal transition (EMT) of breast cancer cells. The applied methods encompassed plasmid transfection, Transwell assay, wound-healing assay, Western blot analysis, co-immunoprecipitation (Co-IP), and rescue assay. For the analysis of CCNL1-related factors and pathways, bioinformatics platforms including Metascape and HURI were also employed. CCNL1 is highly expressed in breast cancer cells and is associated with a poor prognosis. CCNL1 overexpression increased breast cancer cell invasion and migration and accelerated proliferation. Overexpression of CCNL1 was found to upregulate the mesenchymal marker Vimentin and downregulate the epithelial marker E-cadherin expression. There is close relationship between CCNL1, the NF-κB and PI3K/AKT signaling pathways. The direct interaction is verified between CCNL1 and DVL3 by Co-IP, indicating a negative correlation between the two proteins. CCNL1 overexpression affects breast cancer cells' paclitaxel sensitivity through the PI3K/AKT pathway. CCNL1 activates the NF-κB signaling pathway through its interaction with DVL3; additionally, it promotes the PI3K/AKT pathway. Together, these two mechanisms enable CCNL1 to exert a regulatory role in the progression of breast cancer. - Source: PubMed
Publication date: 2026/02/03
Zhang DanCheng RunfenGao JiaxinHan JiyuanNi ChunshengWang SongZhao XiulanSun BaocunLiu Tieju