Canine Protein kinase C,PKC ELISA Kit
- Known as:
- Canine Protein phosphorylation catalyst C,PKC Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- e0010ca
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Bioassay Technology Laboratory
- Gene target:
- Canine Protein kinase PKC ELISA Kit
Related genes to: Canine Protein kinase C,PKC ELISA Kit
- Gene:
- ANKK1 NIH gene
- Name:
- ankyrin repeat and kinase domain containing 1
- Previous symbol:
- -
- Synonyms:
- X-kinase
- Chromosome:
- 11q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-13
- Date modifiied:
- 2013-01-10
Related products to: Canine Protein kinase C,PKC ELISA Kit
Related articles to: Canine Protein kinase C,PKC ELISA Kit
- Obesity has been increasing at an uncontrolled rate. Genetic variations have been shown to contribute to a higher risk of developing the condition, due to impaired satiety regulation, predisposition to addictive eating behaviors, or even specific personality traits. This study aimed to evaluate the influence of gene polymorphisms related to the dopaminergic system on developing severe obesity. - Source: PubMed
Publication date: 2026/04/16
Teixeira Myrela RibeiroFelício Rafaela de Freitas MartinsAssis Izadora Sthephanie da SilvaGouvea Laura WendlingAbreu Gabriella MedeirosSouza Ritiele Bastos dePalhinha LohannaJunior Mario Camposde Mello Neto Cícero BrasileiroMaya-Monteiro Clarissa MenezesBozza Patrícia TorresCarneiro João Regis IvarZembrzuski Verônica MarquesSalum Kaio Cezar Rodriguesda Fonseca Ana Carolina ProençaKohlrausch Fabiana Barzotto - The present study aimed to: (i) compare a patient group with solely alcohol use disorder (AUD) to a group with poly-substance use disorder (poly-SUD) regarding sociodemographic background, morbidity, mortality, and the prevalence of the A1 allele of the Taq1A polymorphism. (ii) Investigate whether gender, age, poly-SUD, and the prevalence of the A1 allele or interactions among these factors, are associated with mortality risk over an 18-year follow-up period. - Source: PubMed
Rauwolf Kerstin KBerggren UlfBalldin JanHasselgren Bune CarolineBerglund Kristina J - The role of neurotransmitter systems in the pathology and management of psychiatric disorders is well documented. Targeting these systems has remained the mainstay of standard pharmacological interventions, with typical and atypical antipsychotics demonstrating effectiveness in reducing both positive and negative symptoms of schizophrenia. However, their clinical efficacy and side effect profiles vary among individuals due to genetic differences. This review aims to examine key genetic variants in the dopaminergic neurotransmitter system that influence antipsychotic response, with particular emphasis on clinically relevant single-nucleotide polymorphisms (SNPs), to support improved treatment outcome prediction and precision psychiatry. Polymorphisms in genes encoding dopamine receptors, transporters, and metabolising enzymes have been associated with variability in antipsychotic efficacy and susceptibility to adverse effects. Across multiple studies, the catechol-O-methyltransferase (COMT) Val158Met (rs4680) polymorphism and the dopamine D2 receptor/ANKK1 Taq1A (rs1800497) variant are among the most consistently reported genetic contributors to variability in dopamine signalling, receptor availability, and drug metabolism. These variants have been linked to differential therapeutic outcomes, including improved response in some treatment-resistant patients, as well as an increased risk of extrapyramidal symptoms, hyperprolactinaemia, and metabolic disturbances. These findings indicate that genetic variation in the dopaminergic system is a key contributor to differences in antipsychotic response. Integrating pharmacogenomic information in clinical practice may enhance personalised treatment strategies, reduce trial-and-error prescribing, and improve long-term outcomes in schizophrenia. - Source: PubMed
Publication date: 2026/03/27
Olasore Holiness S AOlawale Matthew OAsiwaju Damilare POlashore Anthony A - Suicidal behavior is a multifactorial and highly heritable phenotype; however, data concerning its genetic determinants in disparate ethnic groups remain limited. Genes implicated in serotonergic neurotransmission and stress response regulation are regarded as primary candidates for elucidating biological vulnerability to suicide. The objective of this study is to investigate the relationship between suicide attempts and candidate gene polymorphisms in an ethnically homogeneous Kazakh population from Astana, Kazakhstan. The study's sample population comprised 126 patients with a documented history of suicide attempts and 120 age- and gender-matched controls without a history of suicidal behavior. A comprehensive genotyping analysis was conducted, encompassing polymorphisms in genes associated with serotonergic signaling, stress response, and neuroplasticity (, , , , , , , , , , and ). The associations were assessed across several genetic models, using odds ratios with 95% confidence intervals. A substantial correlation was identified between the polymorphism and suicide attempts. The CC genotype exhibited a protective effect ( = 1.36 × 10), while the TT genotype was associated with an elevated risk (OR = 3.16; 95% CI: 1.72-5.81). The association remained robust after stratification by sex, with an even stronger effect observed in women (OR = 4.70; 95% CI: 2.08-10.64). A nominal sex-specific association was observed for the variant, suggesting a potential role in stress-response mechanisms in women; however, this association was no longer statistically significant after adjustment for multiple comparisons. These results identify as a potential genetic marker of suicide risk in the Kazakh population and support the involvement of serotonergic receptor regulation in the biological mechanisms underlying suicidal behavior. The results underscore the significance of sex-specific genetic influences, thereby enhancing our understanding of the polygenic underpinnings of suicidality. - Source: PubMed
Publication date: 2026/02/28
Tatayeva RozaTussupova AruzhanNursafina AkmaralZholdybayeva ElenaBazarbayeva ZhannatFedorenko OlgaSembaeva ZhibekTulembaeva AigulSarkulova SauleKarimbayeva Botagoz - Apolipoprotein E (ApoE) is the primary, most abundant apolipoprotein of the CNS and plays an important role in brain metabolism and lipid homeostasis. In the CNS, ApoE is primarily secreted by astrocytes under homeostatic conditions and by microglia in certain disease-related conditions. APOE has three major alleles: APOE2, APOE3, and APOE4. APOE4 is the strongest genetic risk factor for late-onset Alzheimer's disease (AD), and APOE2 results in decreased risk relative to APOE3. ApoE derived from astrocytes and microglia have been hypothesized to play different roles in the disease pathogenesis of AD. In this study, we profiled the lipidome and proteome of ApoE lipoproteins secreted by astrocytes or microglia and found that they differed according to the cellular source of ApoE and the ApoE isoform. Lipidomics revealed that microglia-derived ApoE lipoproteins were enriched in cholesteryl esters, whereas astrocyte ApoE lipoproteins were enriched in SM. Proteomics revealed that astrocyte ApoE lipoproteins were enriched in proteins involved in glucose metabolism and acute phase response. Microglia-secreted lipoproteins were enriched in proteins involved in complement activation, synapse pruning, proteolysis, and the innate immune response. Further comparison of ApoE lipoproteins from APOE4 microglia revealed that ApoE4 lipoproteins were enriched in complement component 1q and Lpl compared with ApoE2 and ApoE3 microglial lipoproteins, which were enriched in Ankk1 (ankyrin repeat and kinase domain containing 1) and apolipoprotein C1. These results provide the molecular foundation for better understanding of how ApoE functions as an apolipoprotein with the lipoprotein cargo being dependent on the cellular source and ApoE isoform, ultimately contributing to CNS homeostasis and disease pathogenesis. - Source: PubMed
Publication date: 2026/02/13
Strickland Michael RWang ZhenGolden Lesley RWang HuLu PingRen YingxueTabor G TravisZhao NaUlrich Jason DHan XianlinPeng JunminHoltzman David M