KIF2A polyclonal antibody
- Known as:
- KIF2A pab (anti-)
- Catalog number:
- PAB12407
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- KIF2A polyclonal antibody
Related genes to: KIF2A polyclonal antibody
- Gene:
- KIF2A NIH gene
- Name:
- kinesin family member 2A
- Previous symbol:
- KIF2
- Synonyms:
- HK2
- Chromosome:
- 5q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-05-09
- Date modifiied:
- 2016-10-05
Related products to: KIF2A polyclonal antibody
Related articles to: KIF2A polyclonal antibody
- γ-TuRC is the primary microtubule (MT) nucleator in eukaryotic cells. Vertebrate γ-TuRC is composed of γ-tubulin and the γ-Tubulin Complex Proteins (GCPs): GCP2, GCP3, GCP4, GCP5, and GCP6. γ-TuRC localizes to MT-Organizing Centers (MTOCs) and promotes MT nucleation by providing a structural template that mirrors the 13-protofilament symmetry of the MT lattice. To understand the contribution of individual γ-TuRC subunits in mitotic spindle dynamics, we endogenously tagged GCP2, GCP4 or GCP6 with an Auxin-Inducible Degron (AID) tag, enabling precise and rapid depletion of each protein. When depletion occurred before mitotic entry, we observed that cells arrested in prometaphase and that loss of any single subunit resulted in displacement of all γ-TuRC components from spindle poles. In cells with preformed spindles, depletion triggered rapid spindle collapse, demonstrating that γ-TuRC remains essential for the maintenance of spindle integrity. Remarkably, depletion of KIF2A, a MT-depolymerizing kinesin, rescued spindle collapse after γ-TuRC loss, suggesting that KIF2A activity contributes to the spindle instability observed in the absence of γ-TuRC. These findings indicate a dual role of γ-TuRC in mitosis: acting not only as a critical MT nucleation factor for initiation of spindle assembly but also as a stabilizing and capping structure at the minus ends of spindle MTs to preserve spindle integrity. - Source: PubMed
Publication date: 2026/04/11
Aljumaah RehamTurcotte Elizabeth ASundararajan SanjanaAksenova VasilisaArnaoutov AlexeiDasso Mary - The spatial distribution and dynamics of double-strand break (DSBs) repair controlled by microtubules are essential for preserving genomic stability. However, the processes through which extranuclear microtubules govern intranuclear DSB repair across the nuclear envelope (NE) remain poorly understood. This study uncovers a mechanism by which the microtubule-depolymerizing kinesin KIF2A regulates nonhomologous end joining (NHEJ) repair by mediating NE invagination. Our investigation reveals that damage-induced α-tubulin tyrosination triggers KIF2A binding to microtubules, subsequently inducing NE invagination through the microtubule-the linker of nucleoskeleton and cytoskeleton (LINC) complex and lamin B1. This invagination, in turn, provides a larger region of a stable NHEJ repair environment close to the NE, facilitating efficient NHEJ repair. Loss of KIF2A disrupts the formation of invaginations after DNA damage, impacting the formation of 53BP1 foci. Our study establishes KIF2A-mediated NE invagination as a critical regulator of the intricate relationships among microtubules, NE dynamics, and NHEJ repair, shedding light on a previously obscure pathway crucial for genome stability. - Source: PubMed
Ma YujieZhang TianyiZhou Xiao AlbertXu ZhanzhanZhou JiadongAili AbudureyimujiangLi PeiNie ChenXiong YundongLi XiaomanCao BaoshanLi ShiweiWang Jiadong - : Patients with "driver gene-negative" LUAD lack effective targeted therapies. This study aimed to elucidate the role of the glycolysis pathway in driver gene-negative LUAD to identify key genes and potential therapeutic targets. : Bulk RNA sequencing data from 49 patients with driver gene-negative LUAD were analyzed. The driver gene-negative status of patients was confirmed by immunoblotting. Gene set enrichment analysis (GSEA) was conducted on six hallmark pathways related to glycolysis. Additionally, key genes were identified and a risk score model was constructed. Finally, single-cell RNA sequencing data were processed using the Seurat package for data cleaning, dimensionality reduction clustering, and cell type identification. : GSEA analysis revealed significant enrichment of the glycolysis pathway in driver gene-negative LUAD. Differential expression analysis identified 144 genes associated with the glycolysis pathway. Six glycolysis-related genes (ANKZF1, GPR87, KIF2A, LCT, MIF, SDHC) were identified associated with poor prognosis. Single-cell sequencing analysis validated the key role of MIF in the glycolysis process and revealed a positive feedback regulatory axis between MIF and HIF-1α, which may promoting glycolysis and malignant transformation. : This study elucidated glucose metabolic reprogramming mechanisms and highlighted the MIF-HIF-1α axis as a promising therapeutic target in "driver gene-negative" LUAD, which may offer new avenues for improving outcomes, particularly those lacking conventional targeted therapy options. - Source: PubMed
Publication date: 2025/10/10
Yang Hao-ShuaiLi Yuan-HaoChen QiLuo Hong-HeYu Qi-DuoHan YuZhu WeijieZhang JinLiang Chao-Yang - Microtubules are essential components of the cytoskeleton. Dysfunctions of microtubules and microtubule-associated proteins are prominent features of neurodegenerative disorders. In Alzheimer's disease, changes in microtubule composition and hyperphosphorylation of Tau are more closely related to neurodegeneration than amyloid plaque formation. However, the accumulation of amyloid beta (Aβ) species is the earliest event in Alzheimer's disease pathology and induces Tau toxicity. KIF2A is a microtubule depolarizing kinesin with important roles during cortical development. KIF2A expression is maintained in the mature brain, where it is required for neuronal survival. Here, we used a conditional approach to ablate KIF2A specifically in the adult mouse cortex and hippocampus to assess the impact of KIF2A deletion on neuronal survival and Tau phosphorylation. We found that KIF2A deficiency leads to a reduction of dendritic spine density and maturation associated with cognitive decline, followed by an increase in Tau phosphorylation through MAPK ERK1/2 upregulation. We also studied KIF2A expression in a 5xFAD mouse model and post-mortem human brain tissue. We report that Aβ accumulation alters KIF2A expression in neurons and most importantly, KIF2A protein levels are drastically reduced in patients with Alzheimer's disease, but not in patients with other primary tauopathies. Our results shed light on the relationship between Aβ accumulation, KIF2A deregulation, microtubule dysfunction and enhanced Tau phosphorylation in the context of Alzheimer's disease. - Source: PubMed
Ruiz-Reig NuriaVirosztek MargauxChehade GeorgesSuelves NuriaKyalu Ngoie Zola NathalieSalman YasmineSchakman OlivierKienlen-Campard PascalHanseeuw BernardTissir Fadel - Spinal cord injury (SCI) represents one of the recognized difficulties, and its pathological mechanisms remain unclear. Aberrant regulation of the RNA-binding protein (RBP) and selective splicing are associated with SCI. Nonetheless, the mechanisms of RBP regulation and abnormal selective splicing events associated with SCI are unexplored. The Spinal Cord Injury Group (GSE185301) dataset and human peripheral blood RNA sequencing (GSE151371) dataset were obtained from the Gene Expression Omnibus (GEO) database. High-throughput sequencing data from sham-operated (Ctrl) and spinal cord injury (SCI) mice were subjected to gene expression profiling and genome-wide identification of differential selective splicing events. SCI-associated selective splicing events, differentially expressed cells, and differentially expressed RBPs underwent cellular quantification, principal component analysis, and enrichment analysis. Coexpression analysis was conducted to elucidate the regulatory associations among SCI-related variable splicing events, differentially expressed cells, and differentially expressed RBPs. A total of 1643 alternative splicing events (ASEs), 3128 differentially expressed genes (DEGs), 166 differentially expressed RNA-binding proteins (RBPs), and 6 differential cellular taxa were identified, including mesangial cells, microglia, neuronal cells, oligodendrocyte precursor cells (OPCs), oligodendrocytes, and vascular cells. GO and KEGG analyses revealed that differential ASEs, RBPs, and cells were involved in regulating SCI through various biological pathways. Next, we chose to regulate alternative splicing (RAS), which is mainly enriched in the neurodevelopmental and projection neuron developmental pathways, and screened 10 SCI-associated regulated alternative splicing genes (RASGs), including , , , , , , , , , and . Second, the correlation analysis between differential cellular taxa and differentially expressed RBP events identified a total of 12 RBPs significantly associated with cellular taxa and 4 RBPs associated with SCI. The construction of a cellular-RBP-RAS regulatory network revealed the regulatory mechanisms associated with RBPs post-SCI. These RBPs, including Nkrf, Marcks, NDRG4, and Ryr2, were validated in a human peripheral blood RNA sequencing dataset 3 days after SCI and may serve as molecular targets for SCI repair. High-throughput data analysis identified differential RAS, RBPs, and immune cells during SCI. A regulatory network of differential RBPs with RAS and cells was established. Four RBPs associated with SCI were identified: Nkrf, Marcks, NDRG4, and Ryr2. These key RBPs may serve as potential targets for the treatment of patients with SCI. - Source: PubMed
Publication date: 2025/08/12
Gu WenboZhang XiaoYuan XiaoyaHu LihongLi XushengLuo DiYuan Haifeng