KIF2C Antibody - C-terminal region (ARP33916_P050)
- Known as:
- KIF2C Antibody - C-terminal region (ARP33916_P050)
- Catalog number:
- arp33916_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KIF2C Antibody - C-terminal region (ARP33916_P050)
Related genes to: KIF2C Antibody - C-terminal region (ARP33916_P050)
- Gene:
- KIF2C NIH gene
- Name:
- kinesin family member 2C
- Previous symbol:
- KNSL6
- Synonyms:
- MCAK, CT139
- Chromosome:
- 1p34.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-07
- Date modifiied:
- 2014-11-19
Related products to: KIF2C Antibody - C-terminal region (ARP33916_P050)
Related articles to: KIF2C Antibody - C-terminal region (ARP33916_P050)
- The high morbidity and mortality rates of lung cancer associated with smoking underscore the need for a deeper understanding of prognosis-related kinesin family-microRNA-long non-coding RNA-competitive endogenous RNA (KIFs-miRNA-lncRNA-ceRNA) networks. - Source: PubMed
Publication date: 2026/02/27
Kousik Sakshi PriyaSingh JagritiVats PrernaBaweja BhavikaSaini ChainseeNema Rajeev - There is a strong correlation between lactylation, programmed cell death, and the progression of cancer. This study aims to identify prognostic genes associated with lactylation and programmed cell death in pancreatic ductal adenocarcinoma (PDAC), providing new insights for risk stratification and therapeutic strategies. - Source: PubMed
Publication date: 2026/03/12
Zhang BoxingSun GenHuang LuyingWei WenjunYuan YuzhangWang ZehuaPeng XingzhouSong LiangGörgülü KıvançAi Jiaoyu - The difference in molecular characteristics of Triple negative breast cancer (TNBC) aids in distinguishing between its four prominent subtypes- basal-like 1, basal-like 2, mesenchymal, and luminal androgen receptor. This study presents the first integrative framework that combines explainable AI with machine learning approaches to classify TNBC subtypes. Unlike conventional models, our approach offers interpretability while enabling biomarker prioritization by identifying key hub genes that drive subtype-specific predictions. - Source: PubMed
Publication date: 2026/02/22
L Biji CPatel TruptiCharan DevyaniSinha Mangalam GoutamS RupaakJain MedhanshBhardwaj AshutoshGupta AnnanyaJ DheebaK AthiraMishra AnkitaMishra Deepak - Triple-negative breast cancer (TNBC), particularly the androgen receptor-low (AR-low) subtype, is one of the most aggressive and hard-to-treat forms of BC, characterized by a high index of proliferation, chromosomal instability (CIN), and high prevalence of TP53 mutations. These features fuel therapy resistance, metastases, and poor clinical outcomes. An integrated framework describing the dysregulated molecular networks that support the pathobiology of AR-low TNBC is lacking. Multiple published studies in breast cancer have previously proposed mechanistic links between TP53 loss, AR-low states, and heightened FOXM1-driven G2/M transcriptional programs, potentially via deregulation of E2F activity, chromatin-associated co-regulators (e.g., ATAD2), and disruption of repressive networks involving p53-p21-DREAM and SPDEF. Additional reports suggest that FOXM1-associated circuitry may be reinforced by chromatin regulators such as WDR5 and by mitotic/spindle factors such as ASPM, including through feedback interactions and condensate-associated transcriptional organization. We previously showed that FOXM1, a master regulator transcription factor, is upregulated and is a biomarker of poor prognosis in AR-low TNBC. In this study, we filtered a set of "TNBC core genes" known to promote transcriptional chaos downstream of FoxM1. We identified a set of 15 cell cycle regulators-including mitotic kinesin motors (KIF14, KIF11, KIF4A, KIF2C, and KIF20A), centromeric proteins (CENPA, CENPO, CENPL, CENPF, and OIP5), and regulators of proteolysis (UBE2C, UBE2S, UBE2T, PSMD14, and TUBA1B). These 15 genes, which were ranked highly among genes overexpressed in TNBC featured prominently in gene signatures of chromosomal instability and were also overexpressed among AR-low TNBCs and TP53-mutant breast tumors. We show that expression of each of these 15 genes correlates positively with proliferation markers (Ki67, PCNA, and MCM2) in TNBC, and that the overexpression of this gene set is associated with shorter relapse-free survival and distinct immune/stromal infiltration patterns. In light of prior work, our findings point to a FOXM1-associated 15-gene signature enriched in AR-low TNBC and associated with the high-proliferation and high-CIN phenotypes of this clinically challenging tumor type. This 15-gene set represents an actionable vulnerability with therapeutic potential for AR-low TNBC and provides a framework for rethinking how to manage highly proliferative, genomically unstable BCs. - Source: PubMed
Publication date: 2026/02/14
Rida PadmashreeAndreae RaphaelBikhazi NoahJackson BeneciaWang IvanJinna Nikita - Esophageal squamous cell carcinoma (ESCC) accounts for most esophageal cancer cases. This study implemented a multi-dimensional integrative approach to identify tumor-associated autoantibodies (TAAbs) and develop a diagnostic model for the early detection of ESCC. - Source: PubMed
Publication date: 2026/02/10
Zou YuanlinWang HanSong CaijuanWang SirunLi TiandongCheng YifanYe HuaShi JianxiangWang KeyanWang KaijuanSong ChunhuaWang PengZhu Jicun