Chicken ADCY3 (Adenylate Cyclase 3) ELISA Kit
- Known as:
- Chicken ADCY3 (Adenylate Cyclase 3) Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- e-el-ch0362
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Elabscience
- Gene target:
- Chicken ADCY3 (Adenylate Cyclase 3) ELISA Kit
Related genes to: Chicken ADCY3 (Adenylate Cyclase 3) ELISA Kit
- Gene:
- ADCY3 NIH gene
- Name:
- adenylate cyclase 3
- Previous symbol:
- -
- Synonyms:
- AC3
- Chromosome:
- 2p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-22
- Date modifiied:
- 2015-08-26
- Gene:
- ADCY8 NIH gene
- Name:
- adenylate cyclase 8
- Previous symbol:
- ADCY3
- Synonyms:
- HBAC1, AC8
- Chromosome:
- 8q24.22
- Locus Type:
- gene with protein product
- Date approved:
- 1993-02-11
- Date modifiied:
- 2016-10-05
Related products to: Chicken ADCY3 (Adenylate Cyclase 3) ELISA Kit
Human ELC ELISA KIT 96 TEST
OxiSelect In Vitro ROS/RNS Assay Kit (Green Fluorescence), Trial Size
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect Methylglyoxal (MG) Competitive ELISA Kit
OxiSelect TBARS Assay Kit (MDA Quantitation), Trial Size
OxiSelect Total Antioxidant Capacity (TAC) Assay Kit, Trial Size
OxiSelect™ In Vitro ROS RNS Assay Kit (Green Fluorescence), Trial Size(1-3)-beta-D-glucan Sandwich ELISA, Double Antibody(1-Kit )11,12-EET DHET Immunoassay Kit(1-Kit )11,12-EET_DHET Immunoassay Kit(1-Kit) 11,12-DHET Immunoassay Kit(1-Kit) 14,15-DHET Human Urine ELISA Kit(1-Kit) 14,15-DHET Hypertension ELISA Kit(1-Kit) 14,15-DHET sEH activity ELISA Kit(1-Kit) 14,15-EET DHET Hypertension ELISA Kit Related articles to: Chicken ADCY3 (Adenylate Cyclase 3) ELISA Kit
- Adenylate cyclases (ADCYs) catalyze the conversion of ATP to cAMP, an important co-factor in energy homeostasis. Giving ADCYs role in obesity, diabetes and inflammation, we questioned whether calcium-stimulated ADCY isoforms may be variably detectable in human plasma. We report the results of a cross-sectional study assessing circulating levels of functional ADCY1, -3 and -8 in patients with T2D vs. non-diabetic (ND) controls in association with obesity. ADCY1 levels exhibited no significant change between ND and T2D groups. ADCY3 levels were lower in obese individuals, albeit not statistically significantly. In contrast, ADCY8 plasma levels were significantly higher in obese and T2D patients compared to controls ( = 0.001) and patients with T2D only ( = 0.039). ADCY8 levels correlated positively with body mass index and Hb1Ac levels. Parallel to the increased ADCY8 levels, significantly higher cAMP levels were observed in patients with T2D compared with ND controls, and further elevated in obese individuals, irrespective of T2D status. Additionally, cAMP levels positively correlated with fasting plasma glucose levels. In conclusion, the current cross-sectional study demonstrated elevated levels of circulating plasma ADCY8 and cAMP in obesity and T2D. - Source: PubMed
Publication date: 2020/08/24
Abdel-Halim Samy MAl Madhoun AshrafNizam RasheebaMelhem MotasemCherian PreethiAl-Khairi IrinaHaddad DaniaAbu-Farha MohamedAbubaker JehadBitar Milad SAl-Mulla Fahd - Several studies have reported the benefits of olfactory training (OT) in the olfactory nervous system of mouse models. Therefore, in this study we performed next-generation sequencing to evaluate the effects of OT on mRNA sequencing in the olfactory area. - Source: PubMed
Publication date: 2019/02/21
Kim Boo-YoungPark Ju YeonKim Eui JinKim Byung GukKim Sung WonKim Soo Whan - Na,K-ATPase activity in lens epithelium is subject to control by Src family tyrosine kinases (SFKs). Previously we showed hyposmotic solution causes an SFK-dependent increase in Na,K-ATPase activity in the epithelium. Here we explored the role of cAMP in the signaling mechanism responsible for the SFK and Na,K-ATPase response. - Source: PubMed
Shahidullah MohammadMandal AmritlalDelamere Nicholas A - The LH plays a key role in controlling physiological processes in the ovary acting via LH receptor (LHR). In general, the effects of LHR on the regulation of granulosa cell differentiation are mediated mainly via the Gs-protein/adenylyl cyclase/cAMP system; however, the LHR activation could also induce phospholipase C (PLC)/inositol trisphosphate (IP3) via Gq/11 system. Additionally, the expression of G-proteins (GNAS, GNAQ, and GNA11) and PLC β has been showed in bovine antral follicle, concomitant with an increase in LHR expression. To gain insight into the effects of superstimulation with FSH (P-36 protocol) or FSH combined with equine chorionic gonadotropin (eCG; P-36/eCG protocol) on the mRNA expression of proteins involved in LHR signaling in bovine granulosa cells, Nelore cows (Bos indicus) were treated with two superstimulatory protocols: P-36 protocol or P-36/eCG protocol (replacement of the FSH by eCG administration on the last day of treatment). Nonsuperstimulated cows were only submitted to estrous synchronization without ovarian superstimulation. The granulosa cells were harvested from follicles and mRNA abundance of GNAS, GNAQ, GNA11, PLCB1, PLCB, PLCB4, and adenylyl cyclase isoforms (ADCY3, ADCY4, ADCY6, ADCY8, and ADCY9) was measured by real-time reserve transcription followed by polymerase chain reaction. No differences on mRNA abundance of target genes were observed in granulosa cells of cows submitted to P-36 protocol compared with control group. However, the cows submitted to P-36/eCG protocol showed upregulation on the mRNA abundance of target genes (except ADCY8) in granulosa cells. Although the P-36 protocol did not regulate mRNA expression of the proteins involved in the signaling mechanisms of the cAMP and IP3 systems, the constant presence of GNAS, GNAQ, GNA11, PLCB1, PLCB3, PLCB4, and adenylyl cyclase isoforms (ADCY3, ADCY4, ADCY6, and ADCY9) mRNA and the upregulation of these genes in granulosa cells from cows submitted to P-36/eCG protocol reinforce the participation of Gq/11/PLC/IP3 signaling as well as Gs-protein/adenylyl cyclase/cAMP system on LHR pathways during bovine granulosa cell differentiation submitted to superstimulatory treatments. - Source: PubMed
Publication date: 2014/06/16
Castilho A C SNogueira M F GFontes P KMachado M FSatrapa R ARazza E MBarros C M