SIRT2 pAb host: Rabbit
- Known as:
- SIRT2 pAb production species: Rabbit
- Catalog number:
- ap0019
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Bioworld
- Gene target:
- SIRT2 pAb host: Rabbit
Related genes to: SIRT2 pAb host: Rabbit
- Gene:
- PPP1R18 NIH gene
- Name:
- protein phosphatase 1 regulatory subunit 18
- Previous symbol:
- KIAA1949
- Synonyms:
- phostensin
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-02
- Date modifiied:
- 2016-10-05
- Gene:
- SIRT2 NIH gene
- Name:
- sirtuin 2
- Previous symbol:
- SIR2L
- Synonyms:
- -
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-14
- Date modifiied:
- 2016-10-05
Related products to: SIRT2 pAb host: Rabbit
guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) polyclonal antibody'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,β-cyclohexyl-Ala8,D-Tic16,Arg17,Cys18)-Atrial Natriuretic Factor (6-18) amide (mouse, rabbit, rat)
A71915 98% C69H116N26O15S2 CAS:(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Guinea Pig Related articles to: SIRT2 pAb host: Rabbit
- Actinobacillus pleuropneumoniae (APP) is a porcine respiratory pathogen that causes significant economic losses to the global swine industry. APP-induced piglet respiratory disease complex (PRDC) is highly prevalent in winter and triggers an intense inflammatory response in the lungs at disease onset, accompanied by severe infiltration of porcine alveolar macrophages (PAMs). The magnitude of the PAM-mediated immune response following APP infection is a key factor influencing the regression of respiratory disease. However, it remains unclear whether cold stimulation exacerbates this response. In this study, we found that cold stimulation exacerbated APP-induced lung injury and enhanced macrophage activation. Metabolomics and transcriptomics analyses revealed that immune cells underwent metabolic reprogramming in response to energy mobilisation after APP infection, thereby interfering with lung immune function. In addition, we identified silent information regulator 2 (SIRT2) as a key regulator of PAM activation and demonstrated at the molecular level that SIRT2 mediates the immune response to PAMs following APP infection by regulating the acetylation modification of NF-κB p65. In conclusion, our results elucidate the role of SIRT2 in regulating the immune response to PAMs in piglets infected with APP under low-temperature conditions. These findings may provide potential intervention targets and effective control pathways to address the overactivity of immune cells induced by environmental stress and reduce the high incidence of winter respiratory disease in piglets. - Source: PubMed
Publication date: 2026/06/14
Xia RonggeXing WanqunZhu ZhiqiHan QiChen XinpengShi HuiyingWu WencongZhang BoxiLu JingjingGuo WenjingHe LanXu Bin - Aversive memories formed during drug withdrawal can potentiate compulsive drug-seeking behavior. Dynamic rearrangement of the actin cytoskeleton in dendritic spines is crucial for aversive memory formation. We previously discovered that actin polymerization in the dorsal hippocampus plays a key role in this process, yet the molecular mechanisms governing this reorganization remain unclear. - Source: PubMed
Publication date: 2026/06/12
Long Jian-DongYao Song-YuWu Wei-WeiZan Gui-YingWang Zhi-WenWei Xiang-YanShu Xue-LianChen Ye-XiangJu Yun-YueChen JingChai Jing-RuiYe Ru-FengLu Jia-ShuoXu ChiChen ZhongLiu Jing-GenWang Yu-Jun - Negative frequency-dependent selection (FDS) can increase both genetic diversity and population-level mean fitness. While the dual consequence of negative FDS has been theoretically recognized, its genomic basis remains unknown. To explore a genetic link between negative FDS and overyielding, I conducted a genome-wide association study (GWAS) of neighbour genotypic effects on the growth of 98 Arabidopsis thaliana genotypes. By incorporating neighbour genotypic similarity, this GWAS analysis detected the most significant single-nucleotide polymorphism (SNP) on the fifth chromosome of A. thaliana, which was 6 kbp from a known locus responsible for indirect genetic effects. I found negative FDS on the most significant SNP, where individual plants increased their biomass in the presence of neighbours with a dissimilar allele. I also observed overyielding in which a biallelic mixture of the most significant SNP showed a 3% increase in biomass compared with monoallelic conditions. Furthermore, I focused on the genomic region near the most significant SNP and found a signature of balancing selection near a negative regulator of ethylene responses, SIRTUIN 2. The present analysis uncovered a quantitative trait locus linking balanced polymorphisms and overyielding in A. thaliana, providing a proof of principle to understand the maintenance of polymorphism and its positive impact on population productivity. This article is part of the theme issue 'Exploring negative frequency-dependent selection across levels: from genetics to ecology and back again'. - Source: PubMed
Sato Yasuhiro - Pancreatic cancer remains one of the most lethal malignancies, characterised by aggressive progression, metabolic adaptation, and resistance to therapy. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a critical mechanism influencing tumour survival and therapeutic response. However, the role of ferroptosis suppressor genes (FSGs) in pancreatic cancer remains incompletely understood. In this study, FSGs were systematically retrieved from FerrDb V2 and subjected to multi-step filtering to identify a curated set of 196 protein-coding genes. Genomic alteration analysis using cBioPortal across 21 pancreatic cancer studies (n = 5189 samples) identified seven recurrently altered genes (TP53, HSF1, PARP10, ZFP36, SIRT2, ECH1, and ENPP2) with alteration frequencies ≥ 3%. Co-occurrence analysis revealed predominantly cooperative alteration patterns among these genes, suggesting functional complementarity. Survival analysis demonstrated that alterations in FSGs were significantly associated with reduced overall survival in pancreatic cancer, with several genes (ECH1, ZFP36, SIRT2, and ENPP2) showing particularly strong adverse prognostic effects. In contrast, no significant survival associations were observed in oesophageal and gastric cancers, indicating a tumour-specific dependency on ferroptosis-related mechanisms. KEGG pathway enrichment analysis of the broader FSG set revealed significant involvement in pathways related to metabolic regulation (AMPK-mTOR signalling), autophagy, hypoxia response (HIF-1 signalling), and oncogenic signalling (PI3K-Akt pathway). Integration of these findings suggests that ferroptosis suppressor genes contribute to pancreatic cancer progression by promoting metabolic adaptation and resistance to oxidative stress. In conclusion, this study identifies key ferroptosis suppressor genes with prognostic relevance in pancreatic cancer and highlights their integration within critical metabolic and stress-response pathways. The tumour-specific nature of these associations underscores the importance of biological context and supports the potential of FSGs as prognostic biomarkers and potential therapeutic targets in ferroptosis-based strategies. - Source: PubMed
Publication date: 2026/06/10
Singh Nitin KumarSingh ManinderHusain AdilAlnajjar Lina IAhmad FirozMishra Siddhartha KumarAlshamamri NawafSaeed MohdRab Safia ObaidurGupta Varsha - In aquatic invertebrates, hemolymph is critical for host-environment interaction. Although maintaining microbial homeostasis in hemolymph is significant for disease pathogenesis, the key regulatory mechanisms remain elusive. This study investigates the essential role of the respiratory glycoprotein hemocyanin (HMC) in modulating hemolymph microbial composition in penaeid shrimp. Hemocyanin-depleted shrimp infected with (Vp) exhibited disruptions in the niacinamide (NAM) salvage pathway, attenuated plasma niacinamide and nicotinamide adenine dinucleotide (NAD) levels, and reduced transcripts of key enzymes. These alterations correlated with an increased total bacterial load and a higher abundance of opportunistic pathogens like and . Hemocyanin likely modulates niacinamide metabolism through interactions with nicotinamide riboside kinase 1 (NRK1), sirtuin 2 (SIRT2), and sirtuin 6 (SIRT6). Remarkably, niacinamide supplementation after hemocyanin knockdown restored hemolymph microbial balance, reduced dominance, and improved shrimp survival against infection, but not Gram-positive (Sa). These findings provide novel insights into the pivotal role of niacinamide metabolism in regulating shrimp hemolymph microbial composition via hemocyanin. - Source: PubMed
Publication date: 2026/05/07
Bao ShiyuanJiang MingmingAweya Jude JuventusZhang YongshengZhao XianliangZhao YongzhenYang ChunlingLi ShengkangZheng ZhihongZhang Yueling