ADCY2 Antibody (Center)
- Known as:
- ADCY2 Antibody (Center)
- Catalog number:
- AP11322c
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ADCY2 Antibody (Center)
Related genes to: ADCY2 Antibody (Center)
- Gene:
- ADCY2 NIH gene
- Name:
- adenylate cyclase 2
- Previous symbol:
- -
- Synonyms:
- HBAC2, KIAA1060, AC2
- Chromosome:
- 5p15.31
- Locus Type:
- gene with protein product
- Date approved:
- 1993-02-11
- Date modifiied:
- 2016-10-05
Related products to: ADCY2 Antibody (Center)
Related articles to: ADCY2 Antibody (Center)
- Liancheng white ducks have a distinctive "white feathers, black beak, and green feet" phenotype, making them a useful model for studying pigmentation traits in waterfowl. The previous study found that the F1 generation of Liancheng white ducks crossed with white-feathered ducks and hemp-feathered ducks were all gray-black in color. This indicates the specificity and complexity of melanin deposition in Liancheng white ducks, which makes the selection and breeding of pigment traits through phenotyping difficult. The aim of this study was to investigate the candidate transcriptomic regulatory signals of melanogenesis in Liancheng white ducks. Skin, mouth skin, foot skin, liver, and muscle samples were collected from 130-day-old Liancheng white ducks. Morphological differences were observed via histological analysis, and extraction-based pigment levels were determined. The results showed that melanin granules were clearly observed in tissues other than the liver and were distributed mainly in the basal layer of the epidermis and around feather follicles; the pigment values in the tissues decreased in the order mouth skin > liver > foot skin > muscle and skin. However, the relatively high liver value should be interpreted cautiously because obvious melanin granule deposition was not observed histologically. Whole-transcriptome sequencing was performed on mouth skin and skin samples. In total, 3074 differentially expressed genes (DEGs) were screened; upregulated genes associated with melanogenesis included melanocyte inducing transcription factor (MITF) and tyrosinase (TYR); downregulated genes included agouti signaling protein (ASIP) and adenylate cyclase 2 (ADCY2). Eighteen differentially expressed microRNAs (DEmiRNAs) were identified. Based on target prediction and pathway enrichment analysis, novel_290 and apl-miR-11588-3p were identified as candidate miRNAs potentially associated with melanogenesis-related pathways, and their predicted target genes included phosphatidylinositol 3-kinase (PI3K) and Janus kinase 1 (JAK1). Additionally, 364 differentially expressed long noncoding RNAs (DElncRNAs) were identified; TCONS_00063335 and TCONS_00019814 were identified as candidate lncRNAs potentially associated with melanogenesis-related genes, including TYR and TYRP1. A putative ceRNA network was constructed based on the predicted miRNA-mRNA and miRNA-lncRNA relationships, and ENSAPLT00000025522-apl-miR-11588-3p-MAPK8IP3 was identified as a candidate network relationship associated with MAPK-related pigmentation pathways. However, because this relationship was inferred mainly from bioinformatic prediction and expression association analysis, further functional validation is required to confirm whether it contributes to melanogenesis regulation. These findings provide candidate transcriptomic and noncoding RNA information for the further investigation of tissue-specific pigmentation in Liancheng white ducks. - Source: PubMed
Publication date: 2026/06/18
Shi WenliLi LiZhao BangzheCai QiannanLiu XiaopanZhu ZhimingZhang LinliMiao ZhongweiHuang QinlouZheng NenzhuXin Qingwu - This experiment investigated the effects of dietary Krasch. (AOK) supplementation on the n3-polyunsaturated fatty acid (n3-PUFA) profile of subcutaneous adipose tissue (SADT) in Arbas cashmere goats and explored the underlying transcriptional mechanisms. Forty healthy, weaned kids (120 ± 10 days of age; similar body weight) were randomly allocated to two groups ( = 20): a control group (CON, basal diet) and an AOK group (AOK, basal diet with 3% of the roughage replaced by AOK). The feeding trial spanned 104 days, consisting of a 14-day adaptation period and 90 days of data acquisition. Compared with the CON group, AOK significantly reduced the content of saturated fatty acids (SFAs) and n6-polyunsaturated fatty acids (n6-PUFAs)/n3-PUFAs (n6/n3). In contrast, the levels of n3-PUFAs in the SADT of cashmere goats increased markedly ( < 0.05). Compared with the CON group, AOK exhibited significantly higher activities of hormone-sensitive lipase (HSL) ( = 0.027), adenylyl cyclase 2 (ADCY2) ( = 0.010), adenylyl cyclase 5 (ADCY5) ( = 0.046), cluster of differentiation 36 (CD36) ( = 0.013), solute carrier family 27 member 4 (SLC27A4) ( = 0.021), and fatty acid binding protein 4 (FABP4) ( = 0.040), along with significantly lower activities of fatty acid synthase (FAS) ( = 0.002), lipoprotein lipase (LPL) ( = 0.048), and stearoyl-coa desaturase (SCD) ( = 0.026) in SADT. Compared with the CON group, the activities of superoxide dismutase (SOD) ( = 0.032), catalase (CAT) ( = 0.010), glutathione peroxidase (GSH-PX) ( = 0.029), and total antioxidant capacity (T-AOC) ( = 0.002) were significantly increased in the AOK group. Transcriptomic profiling revealed that AOK supplementation downregulated mRNA levels of , 5, , , , 1 (1), stearoyl- 2 (2), 1 (1), 1 (1), (), 1 (1), 1 (1), 27 2 (272), 4 (4), and 1 (1) ( < 0.05). It also markedly induced 4 (4) ( < 0.01) in SADT. Genes significantly enriched in the adenosine-monophosphate-activated protein kinase (AMPK) signaling pathway included , 1, 1, and 1 ( = 0.010). Genes significantly enriched in the phosphatidylinositol 3-kinase-akt (PI3K-Akt) signaling pathway included 1 and 4 ( = 0.015). 1, 2, and 1 were identified as the genes significantly enriched in the insulin resistance signaling pathway ( = 0.048). was the only gene significantly enriched in the cholesterol metabolism pathway ( = 0.049). Genes showing a tendency toward significant enrichment in the peroxisome-proliferator-activated receptor (PPAR) signaling pathway included 4, 1, 1, and ( = 0.051). These interconnected cascades improve insulin sensitivity, stimulate triglyceride (TG) hydrolysis, and modulate n3-PUFA levels. Supplementation with AOK enhances n3-PUFA content by accelerating TG breakdown while simultaneously restraining FA oxidation in SADT. Consequently, AOK supplementation can be effectively used to enhance the nutritional value of cashmere goat meat through improved n3-PUFA deposition in SADT. - Source: PubMed
Publication date: 2026/04/02
Jiang LianguangZhao YanliZhang QingyueZhang ShangxiongGuo XiaoyuGuo YongmeiYan Sumei - To investigate the genetic relationship between irritable bowel syndrome (IBS) and non-alcoholic fatty liver disease (NAFLD). - Source: PubMed
Publication date: 2025/12/15
Hong JundongJi RuiWang PeichengHuang FengmingZhang FanZhou YanlinLv Bin - () is a major foodborne pathogen which can invade intestinal epithelial cells and cause severe systemic infection. Probiotics, as well as their surface layer proteins, hold broad promise for enhancing intestinal barrier function and defending against pathogenic invasion. In the present study, the antagonistic effects of surface layer protein ornithine carbamoyltransferase (OTC) from () WEFA23 against were systematically evaluated in vitro in human intestinal epithelial Caco-2 cells, including assessments of anti-adhesion and anti-invasion capacity, inflammatory cytokine responses, intestinal barrier integrity, and transcriptomic changes, by comparing the effects of wild-type WEFA23 and a previously constructed WEFA23 gene knockout strain ( WEFA23 ). The results demonstrated that WEFA23 achieved significant stronger anti-adhesion and anti-invasion capacity of ( < 0.05) in the presence of OTC, potentially through increasing tight junction protein expression, regulating inflammatory cytokines, and modulating the virulence factors of the pathogen. To elucidate the potential mechanism of the inhibitory effect of OTC protein, RNA-seq was performed. The results revealed that the significantly regulated core differentially expressed genes (DEGs), including , , , and , were found to be involved in γ-aminobutyric acid (GABA)-ergic synapse, calcium, and toll-like receptor signaling pathways. These findings demonstrated that OTC is involved in blocking invasion and revealed the function of the OTC from WEFA23 in antimicrobial and intestinal mucosal defense, providing a conceptual foundation for the development of new probiotic intervention strategies in anti-infection. - Source: PubMed
Publication date: 2025/11/30
He YaoDong BingXie KeHu YingshengHuang YinaTao XueyingWei Hua - Understanding how genomic variants contribute to lung cancer (LC) risk is key to better understanding the molecular mechanisms underlying that risk. While genome-wide association studies (GWAS) have identified numerous LC risk loci, most single nucleotide polymorphisms (SNPs) reside in non-coding regions, making the interpretation of their function challenging. We accounted for lung-specific chromatin interactions and allele-specific gene expression levels in lung tissue to identify novel interactions between LC GWAS SNPs and distal genes. Pathway enrichment analysis implicated eight target genes (CYP2A6, ADCY2, CHRNA3, CHRNA5, LATS1, RAD52, RIF1, TP53BP1) in functional networks involving caffeine metabolism, DNA ionizing radiation (IR)-double strand breaks and cellular response, and nicotine effect on dopaminergic neurons. Novel findings include a role for rs2853677 in ADCY2 dysregulation (previous attribution to TERT) and rs9322193 in targeting tumour suppressor gene LATS1 (previous attribution to RPS18P9/KATNA1). By linking germline variants to more biologically relevant gene targets and somatic processes, our results align more closely with established epidemiological and environmental risk factors for lung cancer, including a potential genetic explanation for the environmental interaction of caffeine and smoking in LC risk. This highlights the value of integrating 3D genome architecture and tissue-specific expression to refine our understanding of cancer susceptibility. - Source: PubMed
Publication date: 2025/11/13
Khoo AldricPudjihartono MichaelO'Sullivan Justin MSchierding William