Browse our anti-BNP (BNP) Antibodies

Pig (Porcine) Brain Natriuretic Peptide (BNP) interaction partners

1. CNP and BNP serve as oocyte maturation inhibitor to inhibit oocyte maturation in mammals

2. ANP and BNP gene expression differs considerably between cardiac chambers in the first 72 hours of life in healthy piglets, resembling the transition from fetal to neonate circulation. The cardiac gene expression does not explain plasma concentrations.

3. Up-regulation of BNP and a reduction in a ratio of sarcoplasmic reticulum calcium ATPase 2a in failing myocardium are observed in a porcine model of tachycardia.

4. serum levels predict mortality in chest pain patients in Argentina

5. Data show that all five molecules, BNP, ICAM-1, TNF-alpha, VCAM-1 and IL-6, quickly and reliably signaled adverse interactions.

6. identification and characterization of a novel alternatively spliced variant of porcine and human NPPB resulting from exon 2 skipping

7. Arial natriuretic factor (ANF) and N-terminal proANF may be better suited than brain natriuretic peptide as markers of cardiac preload during the development and treatment of acute heart failure.

8. Regional differences in BNP and CNP expression were observed in myocardium with sustained left ventricular dyssynchronous contraction.

Mouse (Murine) Brain Natriuretic Peptide (BNP) interaction partners

1. Atopic dermatitis linked cytokine interleukin-31 induced itch is mediated via a NPPB pathway.

2. These results suggested that the papillary tip express a substance that can stimulate BNP production and secretion from cardiomyocytes.

3. This study provides the first evidence of the ability of IL-18 to induce B-type natriuretic peptide synthesis in vitro and outlines the relationship between the two molecules in acute HF patients with an ongoing inflammatory status.

4. The present study provides a novel insight into the potential underlying mechanisms of telmisartan-induced inhibition of cardiomyocyte hypertrophy, which involves inhibition of NFAT activation, nuclear translocation and the ANP/BNP cascade.

5. the developmental regulation and stress response of the Nppa-Nppb cluster involve the concerted action of multiple enhancers and epigenetic changes distributed across a structurally rigid regulatory domain.

6. Data suggest that the negative inhibition of P2X3R activity by the BNP/NPR-A pathway results in a decreased P2X3R-mediated excitability of trigeminal neurons in wildetype cultures. In familial hemiplegic migraine type-1 model cultures, however, lack of efficient P2X3Rs downregulation contributes to the neuronal hyperexcitability phenotype.

7. we have validated a novel gene, Myh14, as a negative regulator of ISO-induced left ventricular mass hypertrophy in an in vivo mouse model and demonstrated the up-regulation of immediate early gene Myc, fetal gene Nppb, and fibrosis gene Lgals3 in ISO-treated Myh14 deficient hearts compared to controls.

8. P2X3 receptors on mouse trigeminal ganglion neurons are subjected to contrasting modulation by inhibitory brain natriuretic peptide and facilitatory calcitonin gene-related peptide that both operate via complex intracellular signaling.

9. mouse trigeminal neurons endogenous BNP acts on NPR-A receptors to determine constitutive depression of P2X3 receptor function. Tonic inhibition of P2X3 receptor activity by BNP/NPR-A/PKG pathways occurs via two distinct mechanisms: P2X3 serine phosphorylation and receptor redistribution to non-raft membrane compartments

10. The findings demonstrated a substantial role of mitochondrial dysfunction in mediating the downregulation of NKCC2 and ENaCalpha in obstructive kidney disease, possibly via iNOS-derived nitric oxide and BNP.

11. Data (including data from studies in knockout mice) suggest expression of ANP/BNP/GC-A (atrial natriuretic peptide, brain natriuretic peptide, and guanylyl cyclase-A) is important in embryonic neovascularization and organogenesis.

12. Goalpha plays a role in ANF sorting during intracellular vectorial transport and with the presence of a mechanism that preserves the molar relationship between cellular ANF and BNP.

13. The RNA-Seq demonstrates that NPPB which well activates natriuretic peptide receptor 1 (NPR1), is well expressed in mouse dorsal root ganglian.

14. a slow modulatory action by BNP on TRPV1 and P2X3 receptors outlining the role of this peptide as a negative regulator of trigeminal sensory neuron excitability to nociceptive stimuli

15. These data provide detailed novel insight into the complex effects of natriuretic peptides and their receptors on electrical conduction in the heart.

16. Natriuretic peptides buffer renin-dependent hypertension.

17. BNP-NPRA signaling is involved in both itch and pain and does not function upstream of the GRP-GRPR dedicated neuronal pathway.

18. Data indicate that the identified stress-responsive enhancer of Nppa and Nppb, the most common markers of heart failure, is a 650-bp fragment within 50 kb of the Nppa and Nppb loci.

19. these results define the primary pruriceptive neurons, characterize Nppb as an itch-selective neuropeptide, and reveal the next two stages of this dedicated neuronal pathway.

20. Elevated BNP levels, by inducing sympathetic overdrive and altering Ca(2+) handling, promote adverse cardiac remodelling and ventricular arrhythmias