ADD2
- Known as:
- ADD2
- Catalog number:
- 001204A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADD2
Related genes to: ADD2
- Gene:
- ADD2 NIH gene
- Name:
- adducin 2
- Previous symbol:
- -
- Synonyms:
- ADDB
- Chromosome:
- 2p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-10-19
- Date modifiied:
- 2015-11-23
Related products to: ADD2
Related articles to: ADD2
- Among the last-resort antibiotics, tigecycline is a semisynthetic drug derivative of tetracycline used in medical facilities, resulting in tigecycline-resistant Acinetobacter baumannii (TRAB) strain development. Recent reports suggested the emergence of heteroresistance, intermediate-resistance, and resistance strain development against the tigecycline of A. baumannii isolates, causing treatment failure in healthcare facilities. In this study, we developed tigecycline-resistant (AbTGC-R) mutants through experimental evolution to investigate the development of moderate resistance in A. baumannii with the reference strain ATCC19606. Clonal populations derived from the evolved lines demonstrated ~ 20-fold resistance against tigecycline. Evolution of resistance against tigecycline did not accompany fitness cost or impact on adherence to abiotic substratum and biofilm-forming potential. The mutants demonstrated cross-resistance against erythromycin and azithromycin. Whole genome sequencing analysis identified mutations in a number of genes, of which adenosine deaminase encoding add2, and a SAM-dependent methyltransferase encoding gstcD (alias trm) were determined to be associated with moderate tigecycline resistance. - Source: PubMed
Publication date: 2026/04/04
Acharya KusumitaBiswas ShatarupaBhattacharyya SayaniGhosh MallikaBhattacharya Arijit - The genetic heterogeneity of autism spectrum disorder (ASD) presents significant challenges in understanding its pathogenic mechanisms, as the genetic risk involves numerous common variants and rare de novo or inherited variants. Prior research has mainly focused on identifying rare variants and their impact on neurodevelopment and neuronal functions in cortical brain regions. By contrast, common variants, which contribute substantially to ASD heritability, remain understudied, suggesting a need to consider both variant types to understand ASD's genetic mechanisms. Previous studies have also implicated subcortical brain regions and peripheral digestive and immune systems, but tissue-specific mechanisms remain unclear. We address these knowledge gaps by identifying gene networks, pathways, and key regulators informed by ASD common variants in brain and peripheral tissues, further examining whether these networks also capture genes informed by rare variants. Our approach integrates genome wide association study (GWAS) summary statistics, tissue-level genetics of gene expression, and gene coexpression and transcriptional regulatory networks across ~50 tissues. Our multitissue, multiomics analysis reveals that key brain regions and networks crucial for synaptic signaling and neurodevelopment are enriched for both rare and common variants, whereas peripheral tissues, such as the digestive and immune systems, are primarily informed by common variants. This partitioning of key tissues and biological pathways into core (targeted by both variant types) and modifying components provide insight into ASD heterogeneity. We also identified central gene network regulators, such as SYT1 and ADD2, which may orchestrate the effects of both common and rare ASD genetic risk factors on ASD pathogenesis. - Source: PubMed
Publication date: 2026/02/06
Gill CameronZuo YanningHa Daniel Sung-MinLittman RussellHong JasonCheng JennyBlencowe MontgomeryWang Susanna Sue-MingHong WeizheWu Ye EmilyYang Xia - In a previous study, we trained, validated and tested models of endometrial cancer (EC) recurrence integrating clinical, genomic and pathological data from the Oncology Research Information Exchange Network (ORIEN). Preliminary studies also have demonstrated that bacterial communities may influence the risk of EC recurrence by altering the local environment within the upper female genital tract. The objective of this study was to evaluate whether extrinsic and environmental factors, including tumor-associated bacterial communities, tumor immune contexture and air pollution alongside clinical, pathologic and genomic features are associated with EC recurrence across clinically relevant risk groups. - Source: PubMed
Publication date: 2026/01/30
Bosquet Jesus GonzalezOsazuwa-Peters OyomoareWagner Vincent MPolio AndrewHoyd RebeccaTarhini Ahmad ACosgrove Casey MHuang Marilyn SCorr Bradley RLeiser Aliza LSalhia BodourDarcy KathleenDood Rob LDockery Lauren ECavnar Michael JLandrum LisaChambers LauraTan Aik ChoonJin NingRounbehler Robert JChurchman Michelle LSpakowicz Dan - Red blood cell (RBC) membranopathies, caused by genetic alterations in membrane and cytoskeletal proteins, lead to significant variability in clinical presentation. This study analyzes 23 single nucleotide variants across nine genes (, and ) in 225 Mexican patients with suspected RBC membranopathies and their effects on hematological parameters. Key variants, such as , , and , were significantly associated with decreased RBC count, hemoglobin levels, packed cell volume, mean corpuscular hemoglobin and/or mean corpuscular hemoglobin concentration. Additionally, the following six combinations showed significant associations with two or three hematological parameters: :c.5992G>C + :c.6046C>A, :c.5992G>C + :c.1378G>T, :c.1378G>T + :c.1797C>T, :c.1378G>T + :c.6793A>G, :c.1797C>T + :c.6793A>G, and :c.410-2550A>G + :c.6531-12C>T. These findings underscore the importance of selected population genetic studies to increase our understanding of genotype-hematological phenotype relationships in RBC membranopathies. - Source: PubMed
Publication date: 2026/02/03
Espinoza-Mata Laura LucíaHerrera-Tirado Isis MarielaBorrayo-López Francisco JavierIbarra-Cortés BerthaPerea-Díaz Francisco Javier - Duodenopancreatic neuroendocrine tumors (dpNETs) are a frequent manifestation in patients with MEN type 1 (MEN1), and metastatic dpNETs are the primary cause of mortality. We evaluated a humoral response in the form of immunoglobulin (Ig)-bound antigens that are associated with dpNET development and progression in patients with MEN1. - Source: PubMed
Publication date: 2026/03/26
Katayama HiroyukiFahrmann Johannes FOlsen CourtneyIrajizad EhsanCai YiningHsiao FuChungDennison Jennifer BPerrier Nancy DHanash Samir M