proline_rich tyrosine kinase 2 (PYK2)
- Known as:
- proline_rich tyrosine phosphorylation catalyst 2 (PYK2)
- Catalog number:
- Z02580
- Product Quantity:
- 10ug
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- proline_rich tyrosine kinase 2 (PYK2)
Related genes to: proline_rich tyrosine kinase 2 (PYK2)
- 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
- Gene:
- PTK2B NIH gene
- Name:
- protein tyrosine kinase 2 beta
- Previous symbol:
- FAK2
- Synonyms:
- CAKB, PYK2, RAFTK, PTK, CADTK
- Chromosome:
- 8p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-22
- Date modifiied:
- 2017-12-06
Related products to: proline_rich tyrosine kinase 2 (PYK2)
Related articles to: proline_rich tyrosine kinase 2 (PYK2)
- 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
Publication date: 2026/06/15
Rojas-Pirela MauraGómez Lesmes Sandra PatriciaSalete-Granado DanielLlorente HernánPérez Nieto María-ÁngelesNovo-Veleiro IgnacioCieza-Borrella ClaraPastor IsabelFernández-Mateos JavierInés Revuelta Sandra MChamorro Antonio-JavierLaso Francisco-JavierGonzález-Sarmiento RogelioMarcos Miguel - Long-term pharmacotherapy is the primary approach for alleviating the symptoms of mental disorders. Numerous pharmacogenomic studies have confirmed that genetic polymorphisms are key factors underlying inter-ethnic and inter-individual differences in drug response. Pharmacogenomic testing is an essential pathway to achieve precision medicine. - Source: PubMed
Publication date: 2026/06/04
Zheng JunZou QiqiWang ChuyanYang QianqianRen JiuyuCao XiangyueWang HuijuanGao Hui - Obesity, characterized by abnormal fat accumulation with comorbidities, continues to increase dramatically, particularly in the pediatric population. Identifying the environmental and genetic causes underlying the development of obesity during early childhood is crucial for establishing preventive and protective treatments for this complex disease. We aimed to investigate genetic variants related to non-syndromic early-onset childhood obesity. - Source: PubMed
Publication date: 2026/04/29
Olgun Celebioglu Hazal BanuOzturk Ayse PinarPoyrazoglu SukranTuncer Feyza Nur - Obesity represents a significant health challenge worldwide, with an increasing trend and high prevalence in Mexico. This metabolic disease, characterized by an increase in body mass index (BMI), leads to abnormal fat accumulation that contributes to several pathologies, and is determined by a complex interaction between diet, lifestyle and genetic factors, such as single nucleotide variants (SNVs) that may influence appetite regulation, adipose tissue function, energy metabolism, reward mechanisms, motivation, food intake behavior control, energy expenditure, fatty acid transport, lipid accumulation, lipolysis, insulin sensitivity, glucose metabolism, among other biochemical processes. However, the frequency of obesity-associated genetic variants remains poorly characterized in Mexican populations-which are highly admixed-as demonstrated by population genetic studies which have established the influence of this admixture in the prevalence and distribution of obesity-related SNVs. - Source: PubMed
Publication date: 2026/04/10
Perezcano CarlosSánchez AndreaCendejas GerardoBorrayo FranciscoPérez-Coria MarianaPérez-Hernández Gerardo