CDHH ELISA kit
- Known as:
- CDHH Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CDHH-Mu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CDHH ELISA kit
Ask about this productRelated genes to: CDHH ELISA kit
- Gene:
- CDH13 NIH gene
- Name:
- cadherin 13
- Previous symbol:
- -
- Synonyms:
- CDHH
- Chromosome:
- 16q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-02-10
- Date modifiied:
- 2014-11-19
Related products to: CDHH ELISA kit
Human ELC ELISA KIT 96 TEST
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Size(1-3)-beta-D-glucan Sandwich ELISA, Double Antibody(1-Kit )11,12-EET DHET Immunoassay Kit(1-Kit )11,12-EET_DHET Immunoassay Kit(1-Kit) 11,12-DHET Immunoassay Kit(1-Kit) 14,15-DHET Human Urine ELISA Kit(1-Kit) 14,15-DHET Hypertension ELISA Kit(1-Kit) 14,15-DHET sEH activity ELISA Kit(1-Kit) 14,15-EET DHET Hypertension ELISA Kit Related articles to: CDHH ELISA kit
- Gliomas are highly invasive primary brain tumors, and additional biomarkers are needed to improve prognostic stratification and clarify the mechanisms underlying tumor invasion. Although α-synuclein (α-syn), encoded by SNCA, is a central protein in neurodegenerative disease, its role in glioma remains poorly defined. - Source: PubMed
Publication date: 2026/09/01
Yu ZhenweiHuang GuoshiYang GengxuanChang QingZhang Jing - Harness racing performance in horses is a complex polygenic trait influenced by genetic background, breeding history, training, and environment. Understanding genomic patterns shaped by long-term artificial selection provides insights into performance-related traits and breed-specific genomic variation. - Source: PubMed
Publication date: 2026/08/25
Moazami IMohammadabadi MAsadollahpour Nanaei HAmiri Ghanatsaman ZMoghbeli Damane MBabenko OBorshch O OleksandrovichIevstafiieva YBuchkovska VKalashnyk OAfanasenko VSlynko V - Suicide is an urgent public health crisis that claimed over 49,000 lives in the US in 2023. While genome-wide association studies of suicide are beginning to reveal genetic risk attributable to common variants with small effects on liability, these results explain only a fraction of the substantial proportion of risk due to genetics known to contribute to suicide mortality. As with other complex health conditions, some of this unexplained genetic risk is likely due to rarer variants with larger effects on liability. Using whole genome sequencing data from 1,054 population-ascertained suicide deaths from the Utah Suicide Mortality Research Study (USMRS) jointly processed with 1,230 controls, we investigated intragenic deletions as a class of genomic variation likely to disrupt gene function. To minimize false positives, deletions were limited to those found in large publicly available control datasets (1000 Genomes, GnomAD, and Centers for Common Disease Genomics) and where replication of deletions occurred across two cohorts within the USMRS suicides. Deletions meeting these filters were manually validated. Eleven deletions had at least 2-fold increase in frequency in suicide deaths vs. controls (range 2.28 to 4.46). Implicated genes were associated with mental health conditions (), epilepsy (), intellectual disability (), neuronal function (), metabolic function (), lipid metabolism (), immune functions (), and Alzheimer's disease (). Pending replication, these results may help prioritize biological pathways for future functional studies with the goal of increasing our understanding of risk mechanisms leading to suicide mortality. - Source: PubMed
Publication date: 2026/07/27
Coon HilaryDiBlasi EmilyNicholas ThomasMonson EricFerris ElliottShabalin AndreyYefimov LoganKeeshin BrooksBakian AmandaHan SeonggyunBaird LisaCallor WilliamStaley MichaelAmaro DierdreLi QingqinWillour Virginia - It is well known that genetic variants contribute to cellular sensitivity to chemotherapeutic agents and ionizing radiation (IR). The aim of this study was to identify single nucleotide polymorphisms (SNPs) and genes associated with the spectrum of normal cellular sensitivity of lymphoblastoid cell lines (LCLs) towards ionizing radiation and mitomycin C (MMC). In the first step, we determined the viability of LCLs established from male participants of the Berlin Aging Study II (BASE-II) aged ≥62 years following treatments with increasing doses of IR (n = 137 cell lines) or MMC (n = 140 cell lines) using the alamarBlue assay. Results from intra-experimental triplicates and three independent experiments for each cell line and treatment were used to calculate the area under the curves (AUCs) representing the specific sensitivity to IR and MMC of each LCL. The data from these experiments were subsequently used as outcomes in genome-wide association studies (GWASs). In addition, we calculated polygenic risk scores (PGS) from UK Biobank GWAS results for four cancer-related phenotypes and assessed the extent to which the variance in the IR and MMC sensitivity is explained by these PGS. The GWAS analyses revealed one variant, rs74728080, located in on chromosome 16, to show genome-wide significant ( < 5 × 10, ß = 2.81) association with cellular viability after treatment with IR. In the GWAS on MMC sensitivity the most interesting signal was elicited by SNP rs113978558 in an intron of the gene on chromosome 1 ( = 9.232 × 10; ß = 1.44). Several other SNPs with statistically suggestive (i.e., < 1 × 10) evidence of association with IR or MMC sensitivity were identified. PGS calculations from GWAS of four cancer-related traits in UKB explained ~5% and ~3% of phenotypic variance in IR- and MMC-induced cell viability, respectively. The genome-wide significant association of rs74728080 with IR sensitivity and the location of this variant in is interesting and functionally highly plausible given its known involvement in oxidative stress response and function as a tumor suppressor. Taken together, our novel data suggest that may be genuinely involved in regulating cellular IR sensitivity. - Source: PubMed
Publication date: 2026/07/30
Schmidt Hannah-LenaOhlei OlenaHerwest SarahSalewsky BastianBertram LarsDemuth Ilja - Hematological adaptation is critical for oxygen transport at high altitudes. While hemoglobin concentration is well-studied, yak (Bos grunniens) hematology versus lowland cattle remains under-explored. We analyzed blood phenotypes from 1244 plateau yaks and 154 lowland cattle. Yaks exhibited elevated hemoglobin, hematocrit, and lymphocyte counts, but reduced platelet counts and monocyte/neutrophil percentages among other parameters, indicating distinct hypoxia adaptation. Using genome-wide association studies (GWAS) and composite of multiple signals (CMS), we identified 6485 selection-associated single-nucleotide variants (SNVs) linked to 43 hematological traits (average 6.85% variance explained). These included 172 yak-selected genes (YSGs), with SLIT3, FSTL5, and PCDH15 showing top pleiotropic effects (SLIT3 regulates immune function and oxygen transport). Thirty-eight YSGs influenced multiple traits, and six (SLIT3, FSTL5, PCDH15, PRIM2, CDH13, HLA-DQB1) overlap with genes under selection in Tibetan highlanders. Crucially, unlike hemoglobin attenuation in humans and other species, yaks show elevated hemoglobin, suggesting an alternative adaptive strategy. Cross-species analysis revealed 76 YSG orthologues affect 13 human blood traits, indicating highland species are likely to have selected the same set of genes for hypoxia adaptation. Our findings demonstrate polygenic, pleiotropic mechanisms underpinning yak adaptation, providing a genomic framework for high-altitude biology and conservation. - Source: PubMed
Sun GuangmingLiu ZiqiJiang HuiLi XinZhang HuiOuzhuluobu Qi XuebinBasangwangdui Ge SiyuWang YimingZheng WangshanZhu Yanbin