Ask about this productRelated genes to: KIF25 antibody
- Gene:
- KIF25 NIH gene
- Name:
- kinesin family member 25
- Previous symbol:
- KNSL3
- Synonyms:
- -
- Chromosome:
- 6q27
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-11
- Date modifiied:
- 2014-11-19
Related products to: KIF25 antibody
Related articles to: KIF25 antibody
- Endometriosis has a significant impact on the social, psychological, psychosomatic, and physical aspects of women's lives. There is increasing evidence that endometriosis has to be seen as a systemic and complex disorder with a multifactorial etiology, accompanied by numerous other pathologies, such as mental disorders and even cancer. Herein, we analyzed Disability-Adjusted Life Years (DALYs) and Years Lived with Disability (YLDs) generated from the Global Burden of Disease Study (GBD 2021), which are key metrics used to measure the worldwide impact of diseases. Besides, differential gene expression data generated from the Turku Endomet Database were calculated. Briefly, log2-transformed gene expression counts were investigated using linear modeling with the function expression ~ condition to generate log2 fold changes and -values for each gene. This enabled a precise comparative analysis of mRNA expression levels between control endometrium and various endometriosis-affected tissues, including ovarian endometrioma, peritoneal lesions, and deep endometriosis. Expression patterns of specific genes related to pain and malignant turnover within endometriosis samples and controls have been analyzed. The identification of upregulated genes like , , , , , , , , and , alongside downregulated genes such as , , , and , highlights a broad transcriptional reprogramming within endometriotic tissues. The clustering analysis, which reveals pain-related genes (/, , , , and ), further solidifies the genetic basis for the chronic and often debilitating pain experienced by patients with endometriosis. In 2021, women with endometriosis experienced the highest rates of total YLDs at 19.98%, with anxiety contributing 17.21% and major depression 8.12%, equating to mean YLDs of 15-24 years. In conclusion, our findings reinforce the need for adopting a holistic, psychosomatic approach to managing endometriosis. The identified genetic markers related to pain provide a biological basis for the profound physical suffering. At the same time, the robust DALYs and YLDs data quantify the devastating impact on mental health, particularly highlighting the significant burden of depression and anxiety. - Source: PubMed
Publication date: 2025/12/23
Kordowitzki PawelKelley Liam PMechsner Sylvia - Human papillomaviruses (HPVs) travel from the trans-Golgi network (TGN) to the condensed (mitotic) chromosomes during mitosis. Partially uncoated HPV capsids utilize a unique vesicular structure for trafficking and nuclear import, which is directed by the minor capsid protein L2. However, it is still unknown which precise factors facilitate post-TGN HPV trafficking to the nucleus. Herein, we analyzed HPV16-infected mitotic cells using high-resolution microscopy, coupled with motor protein inhibition, to further elaborate on post-TGN trafficking by tracking the location and/or quantification of EdU-labeled HPV pseudogenomes on microtubules, certain kinesins, and mitotic chromosomes. We also adapted a knocksideways approach to determine if L2 and Kif11 interact in infected cells. We visualized dynein co-localization with HPV pseudogenomes along mitotic microtubules and measured HPV pseudogenome accumulation after short-term dynein inhibition. Additional inhibitor studies implicated a specific kinesin, Kif11, as participating in HPV pseudogenome delivery to the nucleus. Short-term inhibition of Kif11 decreased HPV pseudogenome accumulation at mitotic chromatin. In addition, Kif11, along with kinesins Kif18a and Kif25, were in proximity to L2 during infection. While we were unable to determine a direct interaction between L2 and Kif11, we were able to show via knocksideways approach that relocalization of exogenous Kif11 decreased HPV pseudogenome accumulation to the mitotic chromatin. Our data support a model whereby HPV16 utilizes dynein for minus-end trafficking along mitotic microtubules and utilizes Kif11 for plus-end movement in the late stage of viral entry. - Source: PubMed
Publication date: 2024/12/04
Keiffer Timothy RDiGiuseppe StephenGuion LucileBienkowska-Haba MalgorzataZwolinska KatarzynaSiddiqa AbidaKushwaha AnandSapp Martin J - Malignant melanoma (MM) is known for its abundance of genetic alterations and a tendency for rapid metastasizing. Identification of novel plasma biomarkers may enhance non-invasive diagnostics and disease monitoring. Initially, we examined copy number variations (CNV) in CDK genes (CDKN2A, CDKN2B, CDK4) using MLPA (gDNA) and ddPCR (ctDNA) analysis. Subsequently, low-coverage whole genome sequencing (lcWGS) was used to identify the most common CNV in plasma samples, followed by ddPCR verification of chosen biomarkers. CNV alterations in CDK genes were identified in 33.3% of FFPE samples (Clark IV, V only). Detection of the same genes in MM plasma showed no significance, neither compared to healthy plasmas nor between pre- versus post-surgery plasma. Sequencing data showed the most common CNV occurring in 6q27, 4p16.1, 10p15.3, 10q22.3, 13q34, 18q23, 20q11.21-q13.12 and 22q13.33. CNV in four chosen genes (KIF25, E2F1, DIP2C and TFG) were verified by ddPCR using 2 models of interpretation. Model 1 was concordant with lcWGS results in 54% of samples, for model 2 it was 46%. Although CDK genes have not been proven to be suitable CNV liquid biopsy biomarkers, lcWGS defined the most frequently affected chromosomal regions by CNV. Among chosen genes, DIP2C demonstrated a potential for further analysis. - Source: PubMed
Publication date: 2024/07/09
Lukacova EHanzlikova ZPodlesnyi PSedlackova TSzemes TGrendar MSamec MHurtova TMalicherova BLeskova KBudis JBurjanivova T - To evaluate the clinical efficacy and safety of Shenzhu Guanxin recipe granules (, SGR) in treating patients with intermediate coronary lesions (ICL), and to investigate the potential mechanism though a transcriptome sequencing approach. - Source: PubMed
Xiao JinBingxin W UMiaoyang LinBiying ZhongLuoqi LinDanping X U - Kawasaki disease (KD) is an acute self-limited febrile vasculitis that mainly affects young children. Coronary artery involvement is the most serious complication in children with KD. It is currently the leading cause of acquired cardiac disease in children from developed countries. Literature data indicate a significant role of genetic susceptibility to KD. The aim of this study was to perform the first Genome-Wide Association Study (GWAS) in a population of Polish children with KD and identify susceptible genes involved in the pathogenesis of KD. The blood samples of Kawasaki disease patients ( = 119) were collected between 2016 and 2020, isolated and stored at the Department of Pediatrics, Nutrition and Metabolic Diseases, Children's Memorial Health Institute in Warsaw. The control group was based on Polish donors ( = 6,071) registered as the POPULOUS collection at the Biobank Lab of The Department of Molecular Biophysics in University of Lodz. DNA samples were genotyped for 558,231 Single Nucleotide Polymorphisms (SNPs) using the 24 × 1 Infinium HTS Human Core Exome microarrays according to the protocol provided by the manufacturer. In order to discover and verify genetic risk-factors for KD, association analysis was carried out using PLINK 1.9. Of all 164,395 variants, 5 were shown to occur statistically (p < 0.05) more frequent in Kawasaki disease patients than in controls. Those are: rs12037447 in non-coding sequence (p = 8.329 × 10, OR = 8.697, 95% CI; 3.629-20.84) and rs146732504 in KIF25 (p = 0.007354, OR = 11.42, 95% CI; 3.79-34.43), rs151078858 in PTPRJ (p = 0.04513, OR = 8.116, 95% CI; 3.134-21.01), rs55723436 in SPECC1L (p = 0.04596, OR = 5.596, 95% CI; 2.669-11.74), rs6094136 in RPN2 (p = 0.04755, OR = 10.08, 95% CI; 3.385-30.01) genes. Polymorphisms of genes KIF25, PTRPJ, SPECC1L, RNP2 may be linked with the incidence of Kawasaki disease in Polish children. - Source: PubMed
Publication date: 2021/02/22
Buda PiotrChyb MaciejSmorczewska-Kiljan AnnaWieteska-Klimczak AnnaPaczesna AgataKowalczyk-Domagała MonikaOkarska-Napierała MagdalenaSobalska-Kwapis MartaGrochowalski ŁukaszSłomka MarcinSitek AnetaKsia Żyk JanuszStrapagiel Dominik