Recombinant Mouse Atrial natriuretic peptide receptor 2 (Npr2), partial

1. The authors show that fibroblast growth factor-induced dephosphorylation of NPR2 decreases its guanylyl cyclase activity in growth plate chondrocytes in living bone. PMID:29199951
2. 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) PMID:28277543
3. NPR2 is involved in FSH-mediated oocyte meiotic resumption, and this process is associated with the EGFR and MAPK3/1 signaling pathways. PMID:26880031
4. NPR2 dephosphorylation in the mural granulosa cells is essential for the normal progression of meiosis in response to LH and EGF receptor activation. PMID:26522847
5. 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. PMID:25473838
6. 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. PMID:25860030
7. 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. PMID:25012822
8. These findings demonstrate that pNPPB may be used as a probe to identify the essential amino acid sequences for activation of NPR2. PMID:24615855
9. GATA2 and Lmo2 cooperatively regulate VEGF-induced angiogenesis and lymphangiogenesis via NRP2. PMID:23892628
10. 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). PMID:23787120
11. 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. PMID:22987720
12. 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. PMID:22696190
13. Cellular exposure to Go6976 reduced basal and natriuretic peptide-dependent, but not detergent-dependent, GC-A and GC-B activity. PMID:21366551
14. These observations suggest that the CNP/GC-B system participates in regulation of adipogenesis, particularly at an early stage in the process. PMID:20603173
15. 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. PMID:20616347
16. findings show mural granulosa cells express Nppc mRNA; cumulus cells surrounding oocytes express mRNA of NPPC receptor NPR2; granulosa cell ligand NPPC and receptor NPR2 in cumulus cells prevent precocious meiotic maturation PMID:20947764
17. regulation by alternative splicing PMID:14514678
18. alterations in the renal CNP/NPR-B system may be an important physiological adjustment when water is scarce PMID:14613785
19. hyperosmotic and lysophosphatidic acid-dependent inhibition of NPRB is mediated by calcium-dependent phosphorylation PMID:15371450
20. A dramatic impairment of endochondral ossification and an attenuation of longitudinal vertebra or limb-bone growth were seen in NPR2 null mice. Female mice were infertile due to the failure of the female reproductive tract to develop PMID:15572448
21. Results show that the dwarf phenotype of the cn/cn mouse is caused by a loss-of-function mutation of the natriuretic peptide receptor 2 gene. PMID:15722353
22. ATP does not activate NPRA and NPRB as has been repeatedly reported. Instead, ATP increases activity primarily by maintaining proper receptor phosphorylation status but also serves a previously unappreciated enzyme stabilizing function. PMID:15911610
23. Data indicate that NPR-B activity represents a significant portion of the natriuretic peptide-dependent guanylyl cyclase activity in the normal heart and accounts for the majority of the natriuretic peptide-dependent activity in the failed heart. PMID:17412809
24. Dwarfism of the short-limbed mouse is caused by the disturbed endochondral ossification, and a mutation in the Npr2 gene. PMID:17728275
25. ATP is not required for the initial activation of natriuretic peptide receptors A and B, but does increase activity over time by reducing the apparent K(m) for GTP. PMID:17848634
26. These data demonstrate that Npr2 and cGKI are essential constituents of the signaling pathway underlying axonal bifurcation at the dorsal root entry zone and neuronal connectivity in the dorsal spinal cord. PMID:17954614
27. Molecular modeling suggested that the conserved arginine is critical for binding to an equally conserved acidic pocket in NPR-B. These results indicate that reduced binding to and activation of NPR-B causes dwarfism in lbab(-/-) mice. PMID:18554750
28. C-type natriuretic peptide (CNP) induces a cGMP signaling cascade via its receptor particulate guanylyl cyclase Npr2 which is essential for sensory axon PMID:19805384

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UNIGENE: Mm.103477

KEGG: mmu:230103

STRING: 10090.ENSMUSP00000030191