Tyrosine kinase receptor A, Human
- Known as:
- Tyrosine phosphorylation catalyst receptor A, Human
- Catalog number:
- Z03106-1
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- Tyrosine kinase receptor Human
Related genes to: Tyrosine kinase receptor A, Human
- 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: Tyrosine kinase receptor A, Human
Related articles to: Tyrosine kinase receptor A, Human
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Publication date: 2026/07/07
Qin ZhenHuoshen WudaLi XueqingLi ShiyuSun ChenYi Sha - Previous studies have demonstrated that exercise can influence motor skill learning. However, the specific components of learning primed by exercise remain unclear. This study examined the effect of a preceding bout of high intensity interval training (HIIT) on the acquisition of a novel motor skill. The investigation focused on whether improvement in skill across the session was attributable to online gains during active practice or offline rest periods between practice blocks. Whether common polymorphisms of the BDNF and DRD2/ANKK1 genes that regulate plasticity, learning, and memory, influenced the relationship between exercise and motor learning was also investigated. HIIT enhanced skill acquisition, but the effects of HIIT priming were not specifically attributable to within-session online or offline learning processes. Contrary to research on overnight consolidation, there was no interaction between BDNF, nor DRD2/ANKK1 genotype, with exercise primed skill learning. This builds our understanding of how exercise benefits skill leaning over a single session. - Source: PubMed
Publication date: 2026/06/26
Brooks EmilyHawi ZiarihHosler JulietKwee JessicaAljehany NerminByblow WinstonHendrikse JoshuaCoxon James - Alcohol use disorder (AUD) is influenced by genetic factors that affect key neurobiological systems, including dopaminergic and GABAergic pathways, which regulate neurobehavioral functions and are modulated by brain-derived neurotrophic factor (BDNF). Variations in these genes contribute to individual vulnerability to AUD. In this study, we investigated single-nucleotide polymorphisms (SNPs) and haplotypic associations in , , and , along with the dopaminergic pathway genes / and , in a Spanish cohort. Peripheral blood-derived genomic DNA was genotyped, and haplotype analyses were conducted. Individual SNPs in , , BDNF, and / showed no significant associations with AUD. In , the rs3219151 T allele was more frequent in AUD patients than in controls (57.9% vs. 49.3%; = 0.03), while the C allele appeared to show a potential protective association. In addition, the GAC haplotype of (rs2197414, rs1992647, rs3219151) was less frequent in AUD than in controls (0.071 vs. 0.122) and showed a protective association (OR = 0.58; 95% CI = 0.34-0.99; = 0.045). Our findings provide exploratory evidence suggesting that specific genetic variants and haplotypes may contribute to AUD susceptibility and support the relevance of multigenic and haplotypic approaches for exploring the neurobiological mechanisms underlying AUD. - Source: PubMed
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