mProX™ Human PRKG1 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 After 8 hours of glucose deprivation, autophagy activation was blunted by Prkg1 knockdown.
Prkg1 was targeted for silencing in CMs, followed by an 8-hour treatment with NG to assess autophagy. Western blots were performed to analyze LC3-II, and corresponding densitometric analyses were conducted (N=4-5).
Ref: Forte, Maurizio, et al. "NPPA/atrial natriuretic peptide is an extracellular modulator of autophagy in the heart." Autophagy 19.4 (2023): 1087-1099.
Pubmed: 35998113
DOI: 10.1080/15548627.2022.2115675
Research Highlights
Micale, Lucia et al. "Downexpression of miR-200c-3p Contributes to Achalasia Disease by Targeting the PRKG1 Gene." International journal of molecular sciences vol. 24,1 668. 30 Dec. 2022.
Achalasia, a disorder affecting the smooth muscle motility of the esophagus, has an unknown origin. Building on prior findings that revealed decreased miR-200c-3p levels in achalasia patient tissues, linked to elevated PRKG1, SULF1, and SYDE1 gene expressions, the objective was to investigate the unexplored interplay between these genes and human miR-200c-3p, shedding light on their potential role in achalasia's development. Employing bioinformatics tools, researchers sought miR-200c-3p binding sites in PRKG1, SULF1, and SYDE1's 3'-UTR. Dual-luciferase assays, quantitative PCR, and immunoblot analysis were conducted, revealing miR-200c-3p's influence on gene expression and hinting at the NO/cGMP/PKG signaling pathway's involvement in achalasia's pathogenesis.
Micale, Lucia et al. "Downexpression of miR-200c-3p Contributes to Achalasia Disease by Targeting the PRKG1 Gene." International journal of molecular sciences vol. 24,1 668. 30 Dec. 2022.
Pubmed:
37767570
DOI:
10.1152/ajprenal.00092.2023
Gotoh, Daisuke. et al. "Impaired nitric oxide mechanisms underlying lower urinary tract dysfunction in aging rats." American journal of physiology. Renal physiology, 2023.
The research aimed to explore changes in bladder and urethral function as well as nitric oxide (NO)-related molecular alterations in aging rats. The rats were categorized into two groups: Group Y, consisting of young rats (12 weeks old), and Group A, comprised of aging rats (15 months old). A 24-hour voiding assessment was conducted, evaluating urodynamic parameters through awake cystometry (CMG) and urethral perfusion pressure (UPP) recordings under urethane anesthesia. They also examined mRNA expression levels of NO-, ischemia-, and inflammation-related markers in bladder and urethral tissues, along with cGMP levels in the urethra. Notably, Group A exhibited significantly higher body weight compared to Group Y. The 24-hour voiding assay yielded inconclusive results. In CMG, Group A showed a significant increase in the number of non-voiding contractions per voiding cycle and post-void residual volume, while voiding efficiency was significantly lower compared to Group Y. UPP recordings revealed significantly reduced urethral pressure and high-frequency oscillation (HFO) amplitude in Group A. Furthermore, the bladder of Group A exhibited significantly higher mRNA expression levels of Hif-1α, Vegf-a, and Tgf-β1, whereas the urethra showed significantly lower mRNA expression levels of Nos1 and Prkg1, along with reduced cGMP concentrations, when compared to Group Y. This research underscores the utility of aging rats as valuable models for studying the natural progression of age-related lower urinary tract dysfunctions, with a likely emphasis on impaired NO-mediated transmitter function as a crucial mechanism.
Gotoh, Daisuke. et al. "Impaired nitric oxide mechanisms underlying lower urinary tract dysfunction in aging rats." American journal of physiology. Renal physiology, 2023.
Pubmed:
37767570
DOI:
10.1152/ajprenal.00092.2023