CciN I
- Known as:
- CciN I
- Catalog number:
- E203
- Product Quantity:
- 200
- Category:
- -
- Supplier:
- SibEm
- Gene target:
- CciN
Related genes to: CciN I
- Gene:
- CCIN NIH gene
- Name:
- calicin
- Previous symbol:
- -
- Synonyms:
- KBTBD14, BTBD20
- Chromosome:
- 9p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-25
- Date modifiied:
- 2016-10-05
Related products to: CciN I
Bos taurus,Bovine,Calicin,CCINBovine calicin (CCIN) ELISA kit, Species Bovine, Sample Type serum, plasmaBovine Calicin(CCIN) ELISA kitBovine Calicin(CCIN) ELISA kitBovine Calicin(CCIN) ELISA kit SpeciesBovineCalicin (CCIN)ELISA Kit , HumanCalicin,CCIN,Homo sapiens,HumanCalicin,Ccin,Mouse,Mus musculusCalicin,Ccin,Rat,Rattus norvegicusCanine Calicin(CCIN) ELISA kitCanine Calicin(CCIN) ELISA kitCCDC99 Gene coiled-coil domain containing 99CcinCCINCcin Related articles to: CciN I
- Precise shaping of the sperm head is essential for successful fertilization, and defects in this process are frequently associated with severe forms of male infertility. Sperm head morphology is coordinated by several testis-specific structures, including the apical ectoplasmic specialization (ES), manchette, and perinuclear theca (PT)-a dense cytoskeletal layer that envelops the nucleus during spermiogenesis. However, the molecular components and physiological functions of the PT remain incompletely understood. This study identified FNDC8 as a testis-enriched protein primarily localized to the PT. Genetic disruption of resulted in male infertility characterized by spermatozoa exhibiting acrosome detachment from the nuclear membrane and sperm head surface collapse. FNDC8 interacted with CCIN and ACTL7A during spermiogenesis, and its depletion destabilized both proteins. Together, these results indicate that FNDC8 is integral to the structural integrity of the PT by mediating protein interactions critical for sperm head morphogenesis, implicating dysfunction as a potential contributor to teratozoospermia in humans. - Source: PubMed
Liu Jia-YiLong Cheng-HongWang Li-YingMa Yan-JieZheng Yun-LongLi WeiWu Bing-BingWu Hong-Bo - Acute myeloid leukemia (AML) is an aggressive blood cancer characterized by poor survival outcomes. Further, due to the extreme molecular heterogeneity of the disease, drug treatment response varies from patient to patient. The variability of drug response can cause unnecessary treatment in more than half of the patients with no or partial therapy responses leading to severe side effects, monetary as well as time loss. Understanding the genetic risk factors underlying the drug response in AML can help with improved prediction of treatment responses and identification of biomarkers in addition to mechanistic insights to monitor treatment response. Here, we report the results of the first Exome-Wide Association Study (EWAS) of ex-vivo drug response performed to date with 175 AML cases and 47 drugs. We used information from 55,423 germline exonic SNPs to perform the analysis. We identified exome-wide significant (p < 9.02 × 10) associations for rs113985677 in CCIN with tamoxifen response, rs115400838 in TRMT5 with idelalisib response, rs11878277 in HDGFL2 with entinostat, and rs2229092 in LTA associated with vorinostat response. Further, using multivariate genome-wide association analysis, we identified the association of rs11556165 in ATRAID, and rs11236938 in TSKU with the combined response of all 47 drugs and 29 nonchemotherapy drugs at the genome-wide significance level (p < 5 × 10). Additionally, a significant association of rs35704242 in NIBAN1 was associated with the combined response for nonchemotherapy medicines (p = 2.51 × 10), and BI.2536, gefitinib, and belinostat were identified as the central traits. Our study represents the first EWAS to date on ex-vivo drug response in AML and reports 7 new associated loci that help to understand the anticancer drug response in AML patients. - Source: PubMed
Publication date: 2025/04/04
Giri Anil KLin JakeKyriakidis KonstantinosTripathi GarimaAlmusa Henrikki - Male infertility manifests in the form of a reduction in sperm count, sperm motility, or the loss of fertilizing ability. While the loss of sperm production can have mixed reasons, sperm structural defects, cumulatively known as teratozoospermia, have predominantly genetic bases. The aim of the present review is to undertake a comprehensive analysis of the genetic mutations leading to sperm morphological deformities/teratozoospermia. - Source: PubMed
Publication date: 2024/10/17
Arora ManviMehta PoonamSethi ShrutiAnifandis GeorgeSamara MarySingh Rajender - We assessed the differences in chemotherapy-induced nausea and vomiting (CINV) severity in patients with breast cancer, receiving neoadjuvant chemotherapy (NAC) and adjuvant chemotherapy (AC). - Source: PubMed
Publication date: 2024/07/13
Son Kyung-LakShin Joon SungLee Sun HyungLee SungwonJung SaimKim Won-HyoungJung DooyoungKim Tae-YongIm Seock-AhLee Kyung-HunHahm Bong-JinYeom Chan-Woo - Male infertility is a common, complex disorder. A better understanding of pathogenesis and etiology is needed for timely diagnosis and treatment. The aim of this study, therefore, was to identify genes involved in the pathogenesis of idiopathic male infertility based on data from transcriptomic level supported with data from genomic level. First, we performed whole gene expression analysis in 20 testis biopsy samples of patients with severely impaired (10) and normal spermatogenesis (10). Further, we have performed systematic review of comparable male infertility studies and overlapped the most significantly expressed genes identified in our study with the most differentially expressed genes from selected studies. Gene Ontology analysis and KEGG functional enrichment have been performed with Enrichr analysis tool. Additionally, we have overlapped these genes with the genes where rare variants have been identified previously. In 10 patients with severely impaired spermatogenesis and 10 controls, we identified more than 1,800 differentially expressed genes ( < 0.001). With the systematic review of three previously performed microarray studies that have met inclusion criteria we identified 257 overlapped differentialy expressed genes (144 downregulated and 113 upregulated). Intersection of genes from transcriptomic studies with genes with identified rare variants revealed a total of 7 genes linked with male infertility phenotype (CYP11A1, CYP17A1, RSPH3, TSGA10, AKAP4, CCIN, NDNF). Our comprehensive study highlighted the role of four genes in pathogenesis of male infertility and provided supporting evidence for three promising candidate genes which dysfunction may result in a male infertility disorder. - Source: PubMed
Publication date: 2023/08/21
Hodžić AlenkaMaver AlešZorn BrankoPetrovič DanielKunej TanjaPeterlin Borut