Ask about this productRelated genes to: KIFC2 Blocking Peptide
- Gene:
- KIFC2 NIH gene
- Name:
- kinesin family member C2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-26
- Date modifiied:
- 2015-08-25
Related products to: KIFC2 Blocking Peptide
Related articles to: KIFC2 Blocking Peptide
- Chronic pain acts as a potent driver of progressive cognitive impairment. Although microglial hyperactivation serves as a pivotal mechanistic bridge in this comorbidity, the intracellular molecular cascades coupling persistent nociception to cognitive decline remain largely elusive. Here, we identify a previously unrecognized microglial secretome remodeling axis, governed by CX3CL1-CX3CR1 signaling, that drives pain-associated cognitive impairment. Clinically, elevated cerebrospinal fluid (CSF) CX3CL1 correlates strongly with cognitive impairment in chronic pain patients. In murine models, pharmacological blockade of the microglial CX3CL1-CX3CR1 signaling attenuated chronic pain-induced memory deficits. Mechanistically, aberrant CX3CL1-CX3CR1 activation triggers a sequential p38 MAPK-NF-κB cascade to upregulate the kinesin motor KIFC2. This KIFC2 surge fundamentally reprograms microglial vesicular trafficking, driving the massive release of IL-17-enriched small exosomes (<100 nm) that subsequently induce synaptic deterioration and neuronal apoptosis manifested by PSD95 degradation, caspase-3 cleavage, and compromised cell viability. Crucially, this microglial p38 MAPK-NF-κB-KIFC2 cascade hyperactivation was validated in situ within the hippocampal slices of chronic pain models. Collectively, our findings delineate a comprehensive cascade spanning from receptor hyperactivation to KIFC2-dependent exosomal remodeling, elucidating a novel mechanism of microglia-mediated neurotoxicity. Targeting this CX3CL1-KIFC2 exosomal axis offers a potential therapeutic strategy to uncouple chronic pain from its debilitating cognitive comorbidities. - Source: PubMed
Publication date: 2026/07/15
Hu ChenZhang XinluZhao WeiKe WenjunMa HaoxiangSang WennaGao Qian - Protein palmitoylation, a reversible post-translational lipid modification, has been implicated in regulating cancer cell signaling and progression; however, its role in prostate cancer (PCa) remains unclear. In this study, we comprehensively analyzed palmitoylation-related genes (PRGs) in PCa by integrating bulk transcriptomic, single-cell RNA sequencing, and spatial transcriptomic datasets. Unsupervised consensus clustering based on PRG expression identified two molecular subtypes with distinct prognoses, immune infiltration profiles, and pathway activities. Differential expression and weighted gene co-expression network analyses revealed five key feature genes, among which KIFC2 was highly expressed in tumor cells and correlated with poor clinical outcomes. The KIFC2 was predominantly enriched in high-grade adenocarcinoma regions. Functional experiments demonstrated that silencing KIFC2 significantly inhibited proliferation and promoted apoptosis in PC3 and DU145 prostate cancer cell lines. Additionally, high KIFC2 expression was associated with increased cell cycle progression and oncogenic signaling pathways, including KRAS and PI3K-AKT. Collectively, these results suggest that palmitoylation and KIFC2 play critical roles in PCa progression and may serve as promising biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/01/10
Huang LiangJiang ShusuanZeng FuhuaZeng GongqianShan Hong - - Source: PubMed
Publication date: 2025/08/02
Liu XinyuLin YuLong WeibingYi RenzhengZhang XiongfengXie ChaoqunJin NaQiu ZiranLiu Xiaobing - Hormone receptor-positive and human epidermal growth factor receptor 2-negative breast cancer (HR+/HER2- BC) is the most common subtype, with a high risk of long-term recurrence and metastasis. Endocrine therapy (ET) combined with cyclin-dependent kinase 4/6 (CDK4/6) inhibitors is a standard treatment for advanced/metastatic HR+/HER2- BC, but resistance remains a major clinical challenge. We report that kinesin family member C2 (KIFC2) was amplified in approximately 50% of patients with HR+/HER2- BC, and its high expression was associated with poor disease outcome, increased tumor protein p53 (TP53) somatic mutation, and active pyrimidine metabolism. Functional assays revealed that depletion of KIFC2 suppressed growth and enhanced sensitivity of HR+/HER2- BC cells to tamoxifen and CDK4/6 inhibitors. Mechanistically, KIFC2 stabilized CDK4 by enhancing its interaction with ubiquitin-specific peptidase 9 X-linked (USP9X). Importantly, reexpression of CDK4 in KIFC2-depleted cells partially rescued the decreased growth and increased sensitivity to tamoxifen and CDK4/6 inhibitors caused by KIFC2 depletion. Clinically, high KIFC2 mRNA expression was negatively associated with the survival rate of patients with HR+/HER2- BC who received adjuvant ET alone or in combination with CDK4/6 inhibitors. Collectively, these findings identify an important role for KIFC2 in HR+/HER2- BC growth and therapeutic resistance, and support its potential as a therapeutic target and predictive biomarker. - Source: PubMed
Publication date: 2025/04/29
Yang Shao-YingJin Ming-LiangAndriani LisaZhao QianLing Yun-XiaoLin Cai-JinHuang Min-YingCai Jia-YangZhang Yin-LingHu XinShao Zhi-MingZhang Fang-LinJin XiCao A YongLi Da-Qiang - Studies suggest that kinesin family (KIF) members can promote the occurrence of colorectal cancer (CRC). However, the mechanism of action has not yet been elucidated. The aim of this study was to identify CRC biomarkers associated with KIF members and to investigate their biological mechanisms in the treatment of colorectal cancer by analyzing multi-omics data. CRC-related datasets and KIF member-related genes (KIFRGs) were used. First, differentially expressed genes (DEGs) and differentially expressed methylation genes (DEMGs) in the TCGA-CRC were identified separately using different expression analyses (CRC vs. control). The intersecting genes were selected by overlapping the DEGs, DEMGs, and KIFRGs. Candidate genes were identified using survival analysis ( < 0.05). Subsequently, based on the candidate genes, biomarkers were selected by gene expression validation and survival analysis. Subsequently, functional enrichment, immune cell infiltration, and drug sensitivity analyses were performed. Single-cell analysis was utilized to perform cell annotation, and then function enrichment and pseudo-temporal analyses were performed. The 12 intersecting genes were identified by overlapping 12,479 DEGs, 11,319 DEMGs, and 43 KIFRGs. The survival analysis showed that Kinesin Family Member C2 (KIFC2) and Kinesin Family Member C3 (KIFC3) had significant differences in survival ( < 0.05). Moreover, KIFC3 passed the gene expression validation and survival analysis validation ( < 0.05); thus, KIFC3 was deemed a biomarker. Subsequently, the pathways involved in KIFC3 were detected, such as the Ecm receptor intersection and chemokine signaling pathway. In addition, we found that KIFC3 was significantly positively correlated with natural killer (NK) cells (r = 0.455, < 0.05) and NK T cells (r = 0.411, < 0.05). Moreover, in the drug sensitivity of the CRC, the potential therapeutic benefits of AZD.2281, nilotinib, PD.173074, and shikonin were detected. Furthermore, using single-cell analysis, 16 cell clusters were annotated, and epithelial cells and M2-like macrophages were enriched in "rheumatoid arthritis". Additionally, we observed that most M1-like macrophages were present in the early stages of differentiation, whereas M2-like macrophages were predominant in the later stages of differentiation. This study identifies KIFC3 as a CRC biomarker through multi-omics analysis, highlighting its unique expression, survival association, immune correlations, and drug sensitivity for potential diagnostic and therapeutic applications. - Source: PubMed
Publication date: 2025/04/02
Wang FenZeng XinxinWen JielunXian KexinJin FengJiang SunfangSun Liyue