A2LD1
- Known as:
- A2LD1
- Catalog number:
- 000853A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- A2LD1
Related genes to: A2LD1
- Gene:
- GGACT NIH gene
- Name:
- gamma-glutamylamine cyclotransferase
- Previous symbol:
- A2LD1
- Synonyms:
- -
- Chromosome:
- 13q32.3
- Locus Type:
- gene with protein product
- Date approved:
- 2008-08-12
- Date modifiied:
- 2017-12-15
Related products to: A2LD1
Related articles to: A2LD1
- Tobacco smoking is a major risk factor for cardiovascular and lung diseases. A better understanding of its neurobiological underpinnings will benefit the prevention of smoking-related illnesses and mortality. Previous studies link smoking to increased iron concentration in the striatum, a central component of the brain's reward system, and to reduced cognitive performance. This study aimed to investigate whether smoking and striatal iron share common biological pathways and to assess potential causal relationships between the two. - Source: PubMed
Publication date: 2026/01/31
Trofimova OlgaIuliani IlariaBergmann Sven - Neoadjuvant chemotherapy (NACT), a key strategy for various cancers, markedly improves patient prognosis and 5-year survival rates. However, numerous patients develop resistance to NACT and thus fail to benefit from it. Therefore, identifying reliable biomarkers to predict patient responsiveness to NACT remains a critical challenge. Here, we demonstrate that elevated expression of INCENP and CDCA8 contributes to poor NACT responsiveness across multiple cancers. Mechanistically, the 5'UTR (GGACT at position 113) of INCENP and the 3'UTR (GGACT at position 1041) of CDCA8 undergo m⁶A methylation and are recognized by YTHDF3, which facilitates their translation through interaction with eIF3A, ultimately driving poor response to NACT. Moreover, inhibition of INCENP and CDCA8 enhances NACT sensitivity by promoting multipolar spindle formation. Collectively, our findings establish that INCENP and CDCA8 serve as crucial biomarkers for predicting NACT responsiveness and as potential therapeutic targets for combination therapy with NACT to improve patient survival. - Source: PubMed
Publication date: 2026/01/21
Wang XiangyuWang TingWang KekeZhang ChengjuanLi ZhiboLiu FeifeiTian XueliShi XiaodanZhang ZihanWang RuiJia LudanLaster Kyle VaughnXia QingxinZhao SiminDong Zigang - Older patients are at risk for acute kidney injury and chronic kidney disease. Age-related increases in DNA methylation at CpG islands have been linked to aging-related diseases like cancer and cardiovascular disease, but the exact causal relationship between methylation in renal aging and other kidney diseases remains unclear. This study aimed to elucidate the methylation status of peripheral blood mononuclear cells (PBMCs) in the Asian population. Using human whole blood DNA methylation analysis from the Taiwan Biobank, we included participants with both whole blood genome-wide methylation data and follow-up data on serum creatinine. We investigated hyper- and hypomethylated genes in comparison of participants with higher and lower estimated glomerular filtration (eGFR) decline rate in overall cohort as well as in comparison of old and young participants in subgroup of participants with higher eGFR decline rate. Common genes and signaling pathways in both comparative analyses were identified. - Source: PubMed
Publication date: 2024/06/15
Yang Po-LungLai Tai-ShuanChou Yu-HsiangLai Liang-ChuanLin Shuei-LiongChen Yung-Ming - Methylation of adenosines at N6 position (m6A) is the most frequent internal modification in mRNAs of the human genome and attributable to diverse roles in physiological development, and pathophysiological processes. However, studies on the role of m6A in neuronal development are sparse and not well-documented. The m6A detection remains challenging due to its inconsistent pattern and less sensitivity by the current detection techniques. Therefore, we applied a sliding window technique to identify the consensus site (5'-GGACT-3') ≥ 2 and annotated all m6A hotspots in the human genome. Over 6.78 × 10 hotspots were identified and 96.4% were found to be located in the non-coding regions, suggesting that methylation occurs before splicing. Several genes, , have been involved in various stages of neuron development and their functioning. However, the contribution of m6A in these genes needs further validation in the experimental model. Thus, the present study elaborates the location of m6A in the human genome and its function in neuron physiology. - Source: PubMed
Publication date: 2021/11/05
Kumar SanjayTsai Lung-WenKumar PavanDubey RajniGupta DeepikaSingh Anjani KumarSwarup VishnuSingh Himanshu Narayan - Events occurring in the chicken caecum following Salmonella Enteritidis infection are relatively well-described. However, mechanisms of the immune response and defence beyond the intestinal tract are less well-described. In this study, we therefore determined changes in protein abundance in the liver and blood serum in response to S. Enteritidis infection using the unbiased approach of shotgun proteomics. Complement and coagulation cascades, TNF signalling, antigen processing and presentation was activated in the liver following infection with S. Enteritidis. Chicken proteins that decreased in the liver were involved in glycolysis, the citrate cycle, oxidative phosphorylation and fatty acid metabolism. No functional category was significantly activated or suppressed in the serum. Concerning individual proteins, VNN1, SAA, AVD, SERPINA3, SERPINB10, AGT, MRP126 or CP increased in abundance both in the liver and serum. MT4, MT3, PTGDS, GLRX and TGM4, though highly inducible in the liver, did not increase in the serum. PIGR, SERPINF2 and IGJ increased in the serum but not in the liver. SERPINA4, apoAIV, CLEC3B, SERPINF1, HRG, AHSG and ALB decreased both in the liver and serum. Avidin-like LOC431660, THRSP, GATM, GGACT, ACOX1, ALDOB or FABP7 decreased in the liver but not in the serum. Finally, CKM, CKB, PLTP, COMP, IGFALS, AMY1A or SERPIND1 decreased in the serum after S. Enteritidis infection but not in the liver. Differently abundant proteins characterise the chicken's response to infection and can be also used as markers of chicken health status. - Source: PubMed
Publication date: 2018/10/21
Polansky OndrejSeidlerova ZuzanaFaldynova MarcelaSisak FrantisekRychlik Ivan