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Human Monoclonal NPPB Primary Antibody for IA, ELISA - ABIN253336
Bu, Zhou, Tang, Jing, Zhang: Expression and purification of a novel therapeutic single-chain variable fragment antibody against BNP from inclusion bodies of Escherichia coli. in Protein expression and purification 2013
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Human Monoclonal NPPB Primary Antibody for IHC, ELISA - ABIN1724677
Dawson, Struthers: Screening for treatable left ventricular abnormalities in diabetic patients. in Expert opinion on biological therapy 2003
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Human Monoclonal NPPB Primary Antibody for IHC, ELISA - ABIN1724675
Pfister, Erdmann, Schneider: [Natriuretic peptides BNP and NT-pro-BNP--the "new troponins" for estimation of heart failure?]. in Deutsche medizinische Wochenschrift (1946) 2003
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Mouse (Murine) Polyclonal NPPB Primary Antibody for IF (p), IHC (p) - ABIN678623
Rigazio, Hernández, Corral: Cardiopathogenic mediators generated by GATA4 signaling upon co-activation with endothelin-1 and Trypanosoma cruzi infection. in Microbial pathogenesis 2014
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Human Monoclonal NPPB Primary Antibody for IP, ELISA - ABIN518426
Chiu, Chen, Su, Lee, Hsieh, Ho: The arrhythmogenic effect of self-assembling nanopeptide hydrogel scaffolds on neonatal mouse cardiomyocytes. in Nanomedicine : nanotechnology, biology, and medicine 2014
Human Monoclonal NPPB Primary Antibody for ELISA (Capture), ELISA - ABIN191150
Crimmins, Kao: A glycosylated form of the human cardiac hormone pro B-type natriuretic peptide is an intrinsically unstructured monomeric protein. in Archives of biochemistry and biophysics 2008
CNP and BNP serve as oocyte maturation inhibitor to inhibit oocyte maturation in mammals
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.
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.
serum levels predict mortality in chest pain patients in Argentina
Data show that all five molecules, BNP, ICAM-1, TNF-alpha, VCAM-1 and IL-6, quickly and reliably signaled adverse interactions.
identification and characterization of a novel alternatively spliced variant of porcine and human NPPB resulting from exon 2 skipping
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.
Regional differences in BNP and CNP expression were observed in myocardium with sustained left ventricular dyssynchronous contraction.
In adult congenital heart disease patients NT-proBNP increased before the occurrence of events, especially in patients who died or developed heart failure.
BNP can independently identify patients with subtle impairment of cardiac function that might benefit from more intensive management.
In patients with hypertension, BNP is superior to ventricular dysfunction on echocardiography in the prediction of risk of major adverse cardiovascular events.
In this review, we summarise the current knowledge of SERCA2a gene therapy for heart failure, analyse potential interaction between BNP levels and therapeutic effects of SERCA2a gene transfer and provide directions for future research to solve the identified problems.
High NT-proBNP levels contribute to increased risk of malnutrition in older patients with heart failure.
two months of mandibular advancement device treatment had no effect on NT-proBNP plasma levels in patients with severe obstructive sleep apnea.
Among patients without heart failure, plasma brain natriuretic level is a strong predictor of death.
This study showed that a higher plasma BNP was associated with a lower left atrial appendage flow velocity in patients with non-valvular atrial fibrillation and normal LV systolic function.
The inclusion of NT-proBNP to the 3C-HF and Seattle heart failure model score resulted in significantly better risk stratification.
In patients with acute exacerbation of COPD, average value of NT-proBNP in patients with left ventricular systolic dysfunction (LVSD) was 3303.2 vs. 1092.5 pg/mL in patients without LVSD.
The polymorphisms of BNP at the rs198389, rs6668352, and rs198388 loci are associated with the occurrence of COPD and COPD with PH, and the occurrence may be related to the abnormal expression level of BNP, Fbg, and Apelin protein in the serum.
increased circulating levels of sTNFR1 and BNP were associated with loss of kidney function in Type 2 diabetic Egyptian patients
Among 3,187 stable coronary artery disease patients with NT-proBNP data, after a 2-year follow-up, NT-proBNP levels were predictive for all-cause death in the stable coronary artery disease population
NTproBNP levels differed among infants who did and did not develop bronchopulmonary dysplasia from 14 to 35 days of life with the greatest difference on day 14 of life. The presence of patent ductus arteriosus did not account for higher levels of NTproBNP at day 14.
In patients with pulmonary arterial hypertension, there appears to be a trend of pro-BNP level increasing immediately after exercise and continuing to be elevated at 1 h. Pro-BNP levels then return to baseline at 2 h post 6 minute walk test.
NT-proANP and NT-proBNP show different sensitivity for phenotypes of atrial fibrillation progression.
Amino-terminal pro-brain natriuretic peptide serum level is associated with catheter-related bloodstream infection in severe burn patients.
BNP is increased in diabetic patients with acute heart failure.
In patients undergoing noncardiac thoracic surgery, we found that an elevated preoperative BNP level (with the level of 59 pg/mL as a cutoff), male gender, and open-chest surgeries were significant risk factors for postoperative atrial fibrillation.
B-type natriuretic peptide levels may predict prognosis in older adults admitted with a diagnosis other than heart failure.
Atopic dermatitis linked cytokine interleukin-31 induced itch is mediated via a NPPB pathway.
These results suggested that the papillary tip express a substance that can stimulate BNP production and secretion from cardiomyocytes.
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.
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.
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.
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.
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.
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.
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
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.
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.
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.
The RNA-Seq demonstrates that NPPB which well activates natriuretic peptide receptor 1 (NPR1), is well expressed in mouse dorsal root ganglian.
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
These data provide detailed novel insight into the complex effects of natriuretic peptides and their receptors on electrical conduction in the heart.
Natriuretic peptides buffer renin-dependent hypertension.
BNP-NPRA signaling is involved in both itch and pain and does not function upstream of the GRP-GRPR dedicated neuronal pathway.
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.
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.
Elevated BNP levels, by inducing sympathetic overdrive and altering Ca(2+) handling, promote adverse cardiac remodelling and ventricular arrhythmias
This gene is a member of the natriuretic peptide family and encodes a secreted protein which functions as a cardiac hormone. The protein undergoes two cleavage events, one within the cell and a second after secretion into the blood. The protein's biological actions include natriuresis, diuresis, vasorelaxation, inhibition of renin and aldosterone secretion, and a key role in cardiovascular homeostasis. A high concentration of this protein in the bloodstream is indicative of heart failure. Mutations in this gene have been associated with postmenopausal osteoporosis.
gamma-brain natriuretic peptide
, natriuretic peptides B
, brain type natriuretic peptide
, natriuretic peptide precursor B
, natriuretic protein
, brain natriuretic peptide
, Brain natriuretic factor
, natriuretic peptide precursor type B
, Gamma-brain natriuretic peptide