anti-Natriuretic Peptide Receptor B/guanylate Cyclase B (Atrionatriuretic Peptide Receptor B) (NPR2) Antibodies

Mouse (Murine) Natriuretic Peptide Receptor B/guanylate Cyclase B (Atrionatriuretic Peptide Receptor B) (NPR2) interaction partners

1. Phosphorylation of specific serine and threonine residues in juxtamembrane regions of Npr2 are required for its enzymatic activity and for axon bifurcation.

2. Myofibrogenesis in cultured Npr2(+/)(-) fibroblasts was insensitive to CNP treatment. Aged Npr2(+/)(-) and Npr2(+/)(-);Ldlr-/- mice developed cardiac dysfunction and ventricular fibrosis. Aortic valve function was impaired in Npr2(+/)(-) and Npr2(+/)(-);Ldlr(-/)(-) mice, with increased valve thickening, myofibrogenesis, osteogenesis, proteoglycan synthesis, collagen accumulation and calcification.

3. elevated in ovaries of polycystic ovary syndrome model

4. It was the aim to investigate the expression of natriuretic peptide receptors NPR-A, NPR-B and NPR-C during adipocyte differentiation (AD), upon stimulation with fatty acids (FA), and in murine and human adipose tissue depots.

5. the present study indicates that CNP and its cognate receptor NPR2 mainly expressed in neurons represent an innate neuroprotective mechanism in neonatal hypoxia-ischemia brain injury.

6. The authors show that fibroblast growth factor-induced dephosphorylation of NPR2 decreases its guanylyl cyclase activity in growth plate chondrocytes in living bone.

7. E2-ERs system was functional in maintaining oocyte meiotic arrest by regulating the expression of natriuretic peptide C and natriuretic peptide receptor 2 (NPPC/NPR2)

8. NPR2 is involved in FSH-mediated oocyte meiotic resumption, and this process is associated with the EGFR and MAPK3/1 signaling pathways.

9. NPR2 dephosphorylation in the mural granulosa cells is essential for the normal progression of meiosis in response to LH and EGF receptor activation.

10. Npr2 is necessary for the precise spatial organization typical of central auditory circuits, but signals are still transmitted with normal timing, and that mutant mice can hear even with these deficits.

11. Npr2 is expressed in hard calluses of wild-type mice, suggesting a possible role of CNP signaling in fracture repair, especially in bone remodeling stage.

12. Data, including data from mutant mice strain Npr2(slw/slw), suggest that Npr2 is critical for fertility but role of Npr2 may be more involved in penile function rather than involved in spermatogenesis.

13. These findings demonstrate that pNPPB may be used as a probe to identify the essential amino acid sequences for activation of NPR2.

14. GATA2 and Lmo2 cooperatively regulate VEGF-induced angiogenesis and lymphangiogenesis via NRP2.

15. Data suggest that epidermal growth factor (Egf)/Egf receptor signaling in cumulus cells (CC) down-regulates Npr2, decreases cGMP, elevates calcium, and induces meiotic resumption/oogenesis in cultured CC-oocyte complexes (in induced meiotic arrest).

16. CNP/NPR2 signaling is essential for oocyte meiotic arrest in early antral follicles and activated LH/amphiregulin/EGFR signaling pathway suppresses this signal by downregulating Nppc expression.

17. NPPC/NPR2 signaling is essential for oocyte meiotic arrest and cumulus oophorus formation, which affects female fertility through the production of oocytes with developmental capacity.

18. Cellular exposure to Go6976 reduced basal and natriuretic peptide-dependent, but not detergent-dependent, GC-A and GC-B activity.

19. These observations suggest that the CNP/GC-B system participates in regulation of adipogenesis, particularly at an early stage in the process.

20. Data suggest that the gastrointestinal tract dysfunction phenotype of slw/slw mice is because of a C-type natriuretic peptide/natriuretic peptide receptor B-signaling defect caused by an Npr2 mutation.

Human Natriuretic Peptide Receptor B/guanylate Cyclase B (Atrionatriuretic Peptide Receptor B) (NPR2) interaction partners

1. It was the aim to investigate the expression of natriuretic peptide receptors NPR-A, NPR-B and NPR-C during adipocyte differentiation (AD), upon stimulation with fatty acids (FA), and in murine and human adipose tissue depots.

2. homozygous mutations in the NPR2 gene underlying variable phenotypes of Acromesomelic dysplasia, type Maroteaux

3. These results of the distinct presence of NPRA and NPRBpositive cells in unstable plaques underlying acute myocardial infarction suggested that natriuretic peptides serve a role in regulating plaque instability in humans.

4. Atenolol treatment normalized the altered expression of Npr1 and Npr2 genes.

5. Data suggest mutations in NPR2 in patients with skeletal overgrowth alter conformation: A488P/R655C missense mutations yield conformation mimicking allosterically activated NPR2; A488P mutation sets phosphorylation as requirement for CNP-dependent activation; R655C mutation abrogates need for phosphorylation; ATP analog inhibits mutants. (NPR2 = atrial natriuretic factor receptor B; CNP = C-type natriuretic peptide)

6. in 4 Indian families with acromesomelic dysplasia, type Maroteaux, 4 homozygous mutations in four different families were identified; these include 3 novel mutations including a deletion frameshift mutation (p.Cys586Ter), one nonsense mutation (p.Arg479Ter), one missense mutation (p.Val187Asp) and one reported missense mutation (p.Tyr338Cys)

7. Heterozygous mutation in NPR2 gene is associated with short stature.

8. Mutations in three genes (GDF5, NPR2, BMPR1B) have been reported to cause different forms of acromesomelic dysplasia

9. IL1R2 hypomethylation and androgen receptor hypermethylation may constitute an important determinant of disease severity, whereas NPR2 hypomethylation and SP140 hypermethylation may provide a biomarker for vulnerability to excessive daytime sleepiness in Obstructive Sleep Apnea

10. Loss-of-function mutations of the NPR2 gene is associated with acromesomelic dysplasia, type maroteaux.

11. Heterozygous mutations in natriuretic peptide receptor-B (NPR2) gene as a cause of short stature

12. NPR2 mutations account for approximately 3% of patients with disproportionate short stature and/or clinical or radiographic indicators of SHOX deficiency and in whom no SHOX defect has been identified.

13. 3 consanguineous families segregating Acromesomelic dysplasia Maroteaux type in an autosomal recessive manner studied. Linkage in the families was established to the NPR2 gene on chromosome 9p12-21. Sequence analysis revealed 2 novel missense variants (p.Arg601Ser; p.Arg749Trp) in 2 families and a previously reported splice site variant (c.2986+2T>G) in the third family.

14. Cardiac fibrosis and the endogenous natriuretic peptide system were evaluated in end-stage heart failure to assess the anti-fibrotic actions of the dual GC-A/-B activator.

15. Overgrowth syndrome associated with a gain-of-function mutation of the natriuretic peptide receptor 2 (NPR2) gene.

16. Gene expression of C-type natriuretic peptide and of its specific receptor NPR-B in human leukocytes of healthy and heart failure subjects

17. Molecular dynamics analysis indicated decreases in the values of Van der Waals, electrostatic energy and potential energy of NPRB/Vasonatrin peptide compared to NPRA/Vasonatrin peptide.

18. Identification of heterozygous dominant negative NPR2 mutations in 2% of Japanese patients with short stature.

19. KIdney NPR2 protein quantity is significantly impacted by genetic variation.

20. study concludes V883M mutation increases maximal velocity in absence of C-type natriuretic peptide (CNP), eliminates requirement for ATP in the CNP-dependent Km reduction and disrupts normal inactivation process; established a molecular mechanism for how an amino acid substitution in GC-B activates the enzyme, which results in abnormally long and fragile bones

Cow (Bovine) Natriuretic Peptide Receptor B/guanylate Cyclase B (Atrionatriuretic Peptide Receptor B) (NPR2) interaction partners

1. These data support the existence of a novel transducing cascade, involving Galpha(q16)beta gamma coupling M(3)AChR to NPR-GC.

2. NPR-B is a highly regulated nano-machinery with domains acting at cross-talk points with other signal transducing cascades initiated by G protein-coupled receptors

3. ATP is not required for the initial activation of natriuretic peptide receptor A and B, but does increase activity over time by reducing the apparent K(m) for GTP.