GAD1 (isoform GAD67)
- Known as:
- GAD1 (isoform GAD67)
- Catalog number:
- Y214095
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- GAD1 (isoform GAD67)
Ask about this productRelated genes to: GAD1 (isoform GAD67)
- Gene:
- GAD1 NIH gene
- Name:
- glutamate decarboxylase 1
- Previous symbol:
- GAD
- Synonyms:
- -
- Chromosome:
- 2q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
Related products to: GAD1 (isoform GAD67)
(Biotin Conjugates) Phospho-Slingshot 1 isoform 1 antibodies Immunogen: peptide Host: Rabbit(FITC-conjugates) Phospho-Slingshot 1 isoform 1 antibodies Immunogen: peptide Host: Rabbit14-3-3 Isoform Panel, Rabbit anti-;14-3-3 protein c-isoform antibody Host rabbit14-3-3 protein c-isoform antibody Ab host: Rabbit14_3_3 Isoform Panel, Rabbit anti_;20 kDa myosin light chain,Homo sapiens,Human,LC20,MLC2,MLC-2C,MRLC1,MYL9,Myosin regulatory light chain 2, smooth muscle isoform,Myosin regulatory light chain 9,Myosin regulatory light chain MRLC1,Myos20 kDa myosin light chain,LC20,MYL9,Myosin regulatory light chain 2, smooth muscle isoform,Myosin regulatory light chain 9,Myosin regulatory light polypeptide 9,MYRL2,Pig,Sus scrofa3_hydroxyisobutyryl_Coenzyme A hydrolase isoform 24-alpha-hydroxy-tetrahydropterin dehydratase 2,Chicken,DCoH-alpha,DcoH-like protein DCoHm,DCOHM,Gallus gallus,Hepatocyte nuclear factor 1a dimerization cofactor isoform,PCBD2,PHS 2,Pterin-4-alpha-carb40S ribosomal protein S4, X isoform,CCG2,Homo sapiens,Human,RPS4,RPS4X,SCAR,SCR10,Single copy abundant mRNA protein40S ribosomal protein S4, X isoform,Mouse,Mus musculus,Rps4,Rps4x40S ribosomal protein S4, X isoform,Rat,Rattus norvegicus,Rps4,Rps4x40S ribosomal protein S4, Y isoform 1,Homo sapiens,Human,PRO2646,RPS4Y,RPS4Y140S ribosomal protein S4, Y isoform 2,Homo sapiens,Human,RPS4Y2,RPS4Y2P Related articles to: GAD1 (isoform GAD67)
- Thoracic aortic dissection (TAD) is a highly lethal vascular condition closely associated with endothelial cell (EC) dysfunction. γ-Aminobutyric acid (GABA) can be synthesized in ECs and modulate cell functions; however, its underlying roles in TADs are unclear. Untargeted metabolomics revealed that GABA levels are decreased in the aortic intima of TAD patients and that GABA is a hub metabolite involved in TAD pathogenesis. To investigate the role of endothelial GABA in TAD progression, mice with EC-specific GAD1 deletion or overexpression were generated via AAV infection, and a TAD model was induced. Both endogenous and exogenous GABA attenuate the development and incidence of TAD by reducing endothelial dysfunction and inflammatory infiltration. Mechanistically, GABA attenuated oxidative stress-induced endothelial dysfunction by inhibiting MAPK/c-FOS signaling pathway activation via GABBR2-mediated mitochondrial homeostasis. Moreover, EC-derived GABA protected vascular SMCs from inflammation-induced disturbances in homeostasis by modulating Notch3 protein expression. Plasma GABA levels are lower in TAD patients than in healthy controls, as determined by ELISA, and correlation analysis revealed that decreased plasma GABA levels are associated with an increased risk of aortic dissection. Diagnostic models for early TAD diagnosis based on plasma GABA levels were constructed and found to be highly effective. These findings demonstrated the substantial benefits of EC-derived GABA for vascular homeostasis by protecting ECs and SMCs from dysfunction and provided new insights for TAD intervention and prevention. - Source: PubMed
Publication date: 2026/04/24
Shao LianboYu YouHuang HaoyueChen YihuanTeng XiaomeiShen HanDing YinglongZhou YihongWang TingyuShen Zhenya - Papillary thyroid carcinoma (PTC) is the most common thyroid malignancy, and cervical lymph node metastasis significantly impacts patient prognosis. This study aimed to develop interpretable artificial intelligence models based on transcriptomics to predict PTC occurrence and cervical lymph node metastasis, while exploring the heterogeneity of risk factors across different regions. We obtained 419 samples from the GEO database, originating from Asia, Europe, and America, comprising 158 normal samples, 203 PTC samples, and 58 metastatic samples. After comparing multiple machine learning algorithms, deep neural networks (DNN) demonstrated superior performance and were used to construct the PTC diagnostic and metastasis predictive models. The optimized PTC diagnostic model achieved an AUC of 0.987 with an accuracy of 0.945, while the PTC metastasis predictive model reached an AUC of 0.998 with an accuracy of 0.987. Model interpretation using SHapley Additive exPlanations (SHAP) and Kolmogorov-Arnold Networks (KAN) methods identified SYT1, REN, CNTN5, and ADAM12 as critical features for PTC diagnosis, whereas COL9A1, CYP4F3, and GAD1 were key predictors for PTC metastasis. Stratification analysis revealed regional differences in risk factors for PTC occurrence, while factors promoting PTC metastasis exhibited commonalities across different regions. Pathway enrichment analysis indicated that regulation of hormone levels and cell population proliferation were common pathways involved in both PTC occurrence and metastasis. Finally, we developed online predictive platforms based on the Streamlit framework to facilitate transparent model exploration and risk estimation. These tools are publicly accessible research-use prototypes intended for model demonstration and interpretability visualization. Because they require standardized gene-expression inputs and have not undergone prospective clinical validation, they should not be used as standalone tools for clinical diagnosis, risk stratification, or treatment decision-making. Overall, our findings identify candidate transcriptomic markers associated with PTC occurrence and lymph node metastasis and provide a basis for future translational evaluation. - Source: PubMed
Publication date: 2026/04/18
Zhang ZhigangLiu HongyuZhao ZhengTan GuoyuZhao YangLiu Xun - Social play behavior is a rewarding behavior predominantly displayed by juveniles of various mammalian species, including humans and rats. Although the mesolimbic reward system is involved in the regulation of social play, how brain regions in this system interact to regulate social play behavior is unknown. Here, we determined the involvement of the ventral pallidum (VP) as well as inputs from the nucleus accumbens (NAc) to the VP in the regulation of social play in male and female juvenile rats. We show that acute pharmacological inactivation of the VP, via microinfusion of the GABA-A receptor agonist muscimol, decreased social play behaviors in both sexes. Next, using Gad1-iCre rats, we show that chemogenetic stimulation of NAc terminals in the VP decreased VP neuronal activation and decreased social play behaviors in both sexes. These findings together indicate that reduced inhibitory NAc input to the VP permits activation of the VP which facilitates the expression of social play behaviors. Lastly, we show that the equal expression of social play behavior in males and females is associated with a male-specific decrease in activation of NAc shell neurons projecting to the VP. This sex-specific change in NAc shell activation following social play exposure eliminated a baseline sex difference in NAc shell activation. In conclusion, these findings may support a model in which the sex-specific modulation of NAc shell inhibitory input to the VP facilitates activation of the VP that is necessary for the typical and equal expression of social play behavior in male and female juvenile rats. - Source: PubMed
Publication date: 2026/04/13
Lee Jessica D AAnderson Daniela NOrsucci Isabella CBowden Samantha MVeenema Alexa H - Metabolic dysfunction is a hallmark of CD8 T cell exhaustion in the tumor microenvironment. Thus, there is growing interest in developing strategies that enhance anti-tumor functions of CD8 T cells via metabolic reprogramming. Here, we identify dipeptidyl peptidase 4 (DPP-4) as a previously unknown regulator of CD8 T cell function and metabolism. We discovered that DPP-4 is upregulated in exhausted CD8 T cells. Pharmacological inhibition of DPP-4 with the FDA-approved anti-diabetic drug sitagliptin transcriptionally and metabolically reprogrammed CD8 T cells, increasing spare mitochondrial respiratory capacity, proliferation, cytotoxic mediator production, and antigen-specific cancer cell killing capability. The functional effects of sitagliptin were dependent on upregulation of glutamate decarboxylase 1 (GAD1), an enzyme that feeds glutamate into the tricarboxylic acid (TCA) cycle, highlighting a new role for GAD1 in CD8 T cell respiration and proliferation. We found that systemic inhibition of DPP-4 in preclinical mouse glioblastoma (GBM) models prolongs survival in a CD8 T cell-dependent manner, and retrospective clinical cohort analysis revealed better outcomes in GBM patients using DPP-4 inhibitors. Importantly, preconditioning of Chimeric Antigen Receptor (CAR) T-cells with DPP-4 inhibition enhanced their cytotoxicity, persistence, and therapeutic efficacy in pediatric GBM. Together, our findings provide mechanistic and biological rationale for repurposing readily accessible DPP-4 inhibitors to enhance anti-tumor CD8 T cell responses. - Source: PubMed
Publication date: 2026/04/03
Teran Pumar Oriana YVanNoy Elton LHaffey AbigailGannamedi Durga PrasadRafie Christine IsabelleHarwood Dylan Scott LykkeBenedetti Julia RBallard Christine Ann PittmanCiervo ErikaCoroa Pedro Henrique Assenza TavaresGrover PayalLeón Brandon EmanuelMitchell JonathanPathak AsmitaColon BrunoGhorayeb Lyenne ElO'Sullivan LauraSaralamma Venu Venkatarame GowdaRuiz Clara LopezKhatwani NatashaKumar SurinderRai PriyamvadaSchatz JonathanShah AshishBinder Zev ACeccarelli MicheleOstrom Quinn TKristensen Bjarne WintherStelekati EriettaWatson Dionysios CLombard David BHaydar DaliaBayik Defne - Depression, anxiety and Insomnia are common among middle school students. Non-suicidal self-injury (NSSI) has become an important mental health issue in this group. This study explores the comorbid relationship between depression, anxiety, and insomnia symptoms among junior high school students from a network perspective and investigates the associations between these symptoms and NSSI. - Source: PubMed
Publication date: 2026/01/12
Qian HangZhang JuanDuan XiangWu Tai-MinXie Yao-FeiYang Bing-XiangLuo DanLiu Lian-ZhongYu Ping