Ask about this productRelated genes to: KIFC3 antibody
- Gene:
- KIFC3 NIH gene
- Name:
- kinesin family member C3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 16q21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-08
- Date modifiied:
- 2016-10-05
Related products to: KIFC3 antibody
Related articles to: KIFC3 antibody
- The distinct features of neonatal megakaryocytes, high proliferation and inefficient platelet production, have clinical repercussions. A diminished capacity for stress thrombopoiesis, the response to acute drops in platelet counts, contributes to the high prevalence of thrombocytopenia in premature infants and to impaired platelet recovery after umbilical cord blood stem cell transplantation. High proliferation also promotes leukemogenesis in babies with Down Syndrome (DS). The transcriptional coactivator Mkl1/MrtfA participates in programming the ontogenic shift from fetal/neonatal to adult-type megakaryopoiesis; in this activity it is opposed by the DS-associated kinase Dyrk1a. In a screen for downstream ontogenic effectors in human progenitors, we identified the kinesin Kifc3 as a factor selectively decreased in adult megakaryocytes and whose knockdown in neonatal megakaryocytes induced adult-type morphogenesis with augmented platelet release. Kifc3 acts as a minus-end directed motor for centrosomal delivery of various cargos. Centrosomal release of Cep192 has recently been found induce cellular process extensions through actin remodeling, reminiscent of megakaryocyte platelet release. In our studies, Cep192 showed striking upregulation and dispersion in adult vs neonatal megakaryocytes, and Kifc3 knockdown recapitulated this effect in neonatal megakaryocytes. A role for Cep192 in promoting megakaryocyte morphogenesis, distinct from its role in centrosome biogenesis, was demonstrated and . screening for Kifc3 inhibitors identified a small molecule that affected neonatal megakaryocytes similarly to Kifc3 knockdown, indicating feasibility for therapeutic targeting of the Kifc3-Cep192 pathway in clinical conditions associated with fetal-type megakaryopoiesis. - Source: PubMed
Publication date: 2026/03/23
Elagib Kamaleldin ELiu SijieBurguener ValentinSahu RanjitKotay Deepika MWatts CiorsdaidhWolber GerhardGoldfarb Adam N - Colorectal cancer (CRC) remains a major global health burden with limited therapeutic options. This study identifies phosphomannomutase 2 (PMM2) as a key oncogenic driver in CRC. PMM2 is significantly upregulated in CRC tissues and cell lines, correlating with advanced tumor stages, lymphatic metastasis, and poor patient survival. Functional assays reveal that PMM2 knockdown inhibits CRC cell proliferation, migration, invasion, and glycolytic activity (reducing glucose uptake, ATP/lactate production, and extracellular acidification rate). Mechanistically, PMM2 interacts with transcriptional regulator TRIM28, promoting TRIM28 nuclear translocation, recruiting transcription factor E2F4, and enhancing KIFC3 transcription by binding to its promoter. KIFC3 mediates PMM2-driven glycolysis, as KIFC3 knockdown partially reverses PMM2-induced metabolic reprogramming and tumor growth in xenograft models. Patient-derived organoid studies further confirm PMM2's role in promoting CRC progression through the PMM2-KIFC3 axis. Collectively, these findings establish PMM2 as a prognostic biomarker and potential therapeutic target in CRC, highlighting its critical role in metabolic reprogramming and tumorigenesis. - Source: PubMed
Publication date: 2026/03/06
Peng ZhengMa BingSong ZhouZhao YunshanYang YangLiu YongLi ChenggangZhang Yong - Invasive non-functional pituitary adenomas (NFPAs) are associated with high recurrence and unfavorable clinical outcomes, yet their underlying molecular mechanisms remain incompletely understood. This study aimed to identify robust biomarkers of invasiveness by integrating transcriptional networks, machine learning, and epigenetic regulation. RNA sequencing was performed on 32 NFPA samples (15 invasive, 17 non-invasive). Weighted gene co-expression network analysis (WGCNA) was used to identify invasiveness-associated modules, which were validated in public datasets (GSE169498, GSE51618). Candidate genes were prioritized using machine learning, and their epigenetic regulation was studied using DNA methylation datasets (GSE207937, GSE115783). We identified a five-gene signature associated with invasiveness (KIFC3, PNMA3, ARHGAP18, LRRC10B, and KCNC4). All five genes were consistently downregulated in invasive NFPAs (all < 0.01) and were enriched in oxidative phosphorylation and neuroactive ligand-receptor interaction pathways. A machine learning validation approach (Random Forest followed by forward stepwise logistic regression) showed strong discriminative performance for this signature (mean AUC = 0.919). DNA methylation analyses indicated no robust differences at the genome-wide level or across promoter regions of the core genes; nevertheless, several locus-specific CpG sites (e.g., near KIFC3) showed suggestive methylation changes. Using an integrative multi-omics framework, we identified a novel five-gene signature associated with NFPA invasiveness. The coordinated downregulation of these genes may reflect alterations in cellular energy metabolism and microenvironmental signaling. Although the signature demonstrated promising diagnostic potential, its transcriptional repression is unlikely to be primarily explained by DNA methylation. These findings provide candidate markers and mechanistic hypotheses for understanding invasive NFPA and developing risk-stratification tools. - Source: PubMed
Publication date: 2026/02/23
Ma XinWu HongyuZhang YuYang ZhijunLiu Pinan - Liver cancer ranks sixth in incidence and third in mortality worldwide, with hepatocellular carcinoma (HCC) accounting for 90% of cases. Kinesin family genes (KIFs) have been implicated in HCC progression, but their specific roles remain unclear. Here, using multiple transcriptomic datasets and machine learning, we systematically screened KIF genes in HCC and identified nine key differentially expressed KIFs (KIF3A, KIF3B, KIF5B, KIF11, KIF13A, KIF13B, KIF20A, KIFC3, KLC2) as diagnostic biomarkers. A logistic regression model showed excellent diagnostic accuracy (AUC = 0.992) in the GSE121248 dataset. Six genes (KIF3A, KIF5B, KIF11, KIF13B, KIF20A, KLC2) were validated in TCGA, several correlating with prognosis. Notably, KIF20A was an independent prognostic factor, validated across cohorts. Single-cell and experimental data revealed high KIF20A expression in HCC cells, promoting proliferation and migration. Mechanistically, KIF20A drives tumor growth and metastasis via Wnt/β-catenin signaling and epithelial-mesenchymal transition (EMT) proteins such as N-cadherin, Slug, Snail, and Twist1/2. Wnt pathway activator SKL2001 and inhibitor LGK974 confirmed KIF20A's role in tumor progression. Upstream, the transcription factor FOXK1 was identified as a key positive regulator of KIF20A. FOXK1 is overexpressed in HCC, strongly correlates with KIF20A, and predicts poor prognosis. ChIP-seq and promoter assays verified FOXK1's direct binding to the KIF20A promoter, activating its transcription. In conclusion, KIF20A serves as a diagnostic and prognostic biomarker promoting HCC progression via Wnt/β-catenin signaling, regulated by FOXK1, offering new therapeutic targets. - Source: PubMed
Publication date: 2026/02/19
Liu JiaxuanZhang MengLi JialingTian YuZhao JinyanLiu Xue - Cervical cancer (CC) remains one of the leading female malignancies. Epithelial cells (EpCs), primarily derived from the cervical squamous and glandular epithelium, are targeted by human papillomavirus to drive CC. Herein, we aimed to develop an EpC-specific risk model to improve clinical outcomes and unravel tumor immune microenvironment alterations in CC. - Source: PubMed
Publication date: 2026/02/06
Wang XueguPan XingchenLi XiangDing BiaoJin ZhixinWang XiaojingDou ChengliNair Sujit