FMP-API-1
Based on 1 Customer Validation
FMP-API-1 is an A-kinase anchoring protein (AKAP)-PKA interaction inhibitor. FMP-API-1 binds to the allosteric site of PKA R subunits and increases the activity of PKA and AQP2 in PKA-knockout cell lines of renal cortical collecting ducts (mpkCCD cells). FMP-API-1 has the potential for the study of nephrogenic diabetes insipidus (NDI).
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Reinheit : 95.51%
- CAS. Nr.: 16523-28-7
- Formel: C13H14N2O2
- Molecular Weight:230.26
-
Speicherung:
-20°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Biologische Aktivität
Beschreibung
Chemical Information
-
CAS. Nr. 16523-28-7
-
Appearance Solid
-
Molecular Weight 230.26
-
Formel C13H14N2O2
-
Color Light yellow to brown
-
SMILES
C1=CC(=C(C=C1CC2=CC(=C(C=C2)O)N)N)O
-
Versand
Room temperature in continental US; may vary elsewhere.
-
Speicherung
-20°C, stored under nitrogen
* In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)
Protokoll
-
Gene Editing
Gene editing modify specific sites within the genome through gene deletions, insertions or conversions to study functionally unknown genes or conduct gene therapy. It is also used to change the biological traits of organisms to establish new varieties. Gene editing techniques include zinc finger nuclease (ZFN), transcription activator-like effector nuclease (TALEN), and clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas 9) (CRISPR/Cas9).
-
Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Reinheit & Dokumentation
-
Data Sheet (266 KB)
-
SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
- Norwegian - NO (393 KB)
- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
-
Handling Instructions (2659 KB)
Verweise
[1]. Ando F. Activation of AQP2 water channels by protein kinase A: therapeutic strategies for congenital nephrogenic diabetes insipidus. Clin Exp Nephrol. 2021 Oct;25(10):1051-1056. [Content Brief]
[2]. Fumiaki Ando, et al. AKAPs-PKA disruptors increase AQP2 activity independently of vasopressin in a model of nephrogenic diabetes insipidus. Nat Commun. 2018 Apr 12;9(1):1411. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)