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anti-Human BDKRB2 Antibodies:
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Human Polyclonal BDKRB2 Primary Antibody for IHC, IHC (p) - ABIN4285141
Niewiarowska-Sendo, Polit, Piwowar, Tworzydło, Kozik, Guevara-Lora: Bradykinin B2 and dopamine D2 receptors form a functional dimer. in Biochimica et biophysica acta 2017
BK receptors, B1 and B2 (BKR-B1 and B2), were also detected in both epithelial and stromal cells of endometriotic lesions. The localization of BKR-B1 was nucleus mainly, whereas BKR-B2 was detected at cytoplasm.
Study results indicated that the bradykinin B2 receptor-mediated pathway is involved in the cPLA2-related inflammatory response from the PKC pathway in traumatic brain injury.
The most characteristic signaling pathways for B2R and D2R, dependent on intracellular Ca(2+) and cAMP concentration, respectively, were analyzed in cells presenting similar endogenous expression of B2R and D2R.The evidence of B2R-D2R dimerization may open new perspectives in the modulation of diverse cellular functions which depend on their activation.
These results indicate that KOR can form a heterodimer with B2R and this leads to increased protein kinase A activity by the CREB signaling pathway, leading to a significant increase in cell proliferation.
Study demonstrated the ability of long-chain polyunsaturated fatty acids to act as agonist to the B2R at nanomolar concentrations and to induce receptor conformational changes.
Data suggest that N-myc (and STAT) interactor (NMI) could improve its downstream target bradykinin B2 receptor (BDKRB2) expression to induce extracellular signal-regulated kinases (ERK) 1/2 activation, and thereby further evoke malignant progression of hepatocellular carcinoma (HCC).
Data show that mRNA and protein of bradykinin type 2 receptors, but not bradykinin type 1 receptors, were abundant in cultured c-Kit+ progenitor cells.
BDKRB2 +9/-9 bp polymorphisms affected the gene expression and nitric oxide production, which were associated with radiographic severity of osteoarthritis, suggesting that the BDKRB2 +9/ -9 bp polymorphisms may act as a genetic modulator of osteoarthritis, and play an essential role in inflammatory process in osteoarthritis.
Review/Meta-analysis: suggest bradykinin B2 receptor -58C allele and -58CC genotype increase the risk of hypertension in Asians and African-Americans. Inversely, -58TT genotype decreases the risk of hypertension in Asians and African-Americans.
authors found significant interactions among PRKCA, NOS3 and BDKRB2 genotypes associated with enalapril responses.
Bronchial B2R expression is constitutively elevated in allergic asthma and is further increased after allergen exposure together with NF-kB expression.
Report the presence of nuclear B2R in the utero-placental unit and reduced abundance of nuclear B2R in extravillous trophoblast in preeclampsia.
Data provide evidence that the BDKRB2 +9/-9 polymorphisms influence pro-inflammatory cytokine levels in knee osteoarthritis by altering TLR-2 expression.
These results suggest that the response to long-term exercise training could be modulated by the BDKRB2 gene -9/+9 polymorphism in male athletes. In well-trained swimmers, BDKRB2 gene variation was not found to be an independent determinant of swimming performance.
Significant association between the -58T/C polymorphism and the increased risk of Hypertension was found in Northern Han Chinese population.
Bradykinin inhibits oxidative stress-induced senescence of endothelial progenitor cells through the B2R/AKT/RB and B2R/EGFR/RB signal pathways.
Bradykinin receptor B2 (B2R) genetic variation may affect thirst because of effects bradykinin activity.
These results indicate that B2R couples with P2Y2R and that these G-protein-coupled receptors act together to fine-tune cellular responsiveness.
The nasal mucosa specimens from chronic rhinosinusitis patients expressed relatively higher B2R and slightly higher kininogen (KNG)/BK and B1R.
A cross-talk was found between bradykinin B2 receptor and cytokines in retinal pigment epithelium.
first evidence indicating the causation between ACE DD or B2R+9bp genotype and the increased risk for diabetic nephropathy, broadening our horizon about the role of genetic modulators in this disease.
B2R signaling promotes aortic rupture within a ApoE-eficient mouse model associated with the ability to stimulate inflammatory phenotypes of neutrophils and vascular smooth muscle cells.
B2R activation occurs in the diabetic skin and delays wound healing. B2R blockade improves skin wound healing in diabetic mice and is a potential therapeutic approach to diabetic ulcers.
role in nephrotoxicity induced by cisplatin therapy
a novel pathway by which C5aR/B2R cross-talk couples transendothelial leakage of plasma proteins to the cytokine circuitry that coordinates antiparasite immunity.
investigated if expression of B1 and B2 kinin receptors can be affected by IL-4 and IL-13; data show, for the first time, that IL-4 and IL-13 decrease kinin receptors in a STAT6-dependent mechanism
B(2) receptor deficiency altered plasma oxidant/antioxidant balance.
Data suggest that nicotine impairs mucosa-dependent Bdkrb2 (bradykinin B2 receptor) mediated trachea relaxation; nicotine also down-regulates tracheal expression of COX2/Ptgs2 (cyclooxygenase 2) and mPGES-1 (microsomal prostaglandin E2 synthase-1).
Data suggest that expression of Bdkrb2 is up-regulated in adrenal medulla as the result of immobilization stress; data from CRH (corticotropin-releasing hormone) knockout mice suggest this up-regulation requires catecholaminergic glucocorticoids.
B1R and B2R receptors exert a critical role in the establishment of persistent hypersensitivity observed in an experimental autoimmune encephalomyelitis model
Data indicate that Bdkrb2(-/-) mice have elevated plasma angiotensin-(1-7) and messenger RNA and protein for its receptor Mas.
A loss of B1 receptors markedly exacerbates the severity of dextran sulfate sodium-induced colitis in mice, which may be associated with compensatory overexpression of B2 receptors
Null mutations at the p66 and bradykinin 2 receptor loci induce divergent phenotypes in the diabetic kidney in mice.
Kinin-B2 receptor activity determines the differentiation fate of neural stem cells.
Data highlighted the role of several altered pathological pathways in response to disruption of B(2)R and to the diabetic state that included.
These findings suggest that activation of the bradykinin/B2R pathway contributes to development of host resistance to visceral leishmaniasis.
Data indicate that under normal sodium intake, epithelial Na(+) channel (ENaC) open probability (P(o)) was modestly elevated in bradykinin receptors B1R, B2R(-/-) mice.
Data conclude that kinin B2 receptors are important for modulation of insulin secretion and for the preservation of normal glucose levels and hepatic functions in obese mice.
Inflammatory muscle pain involves a cascade of events that is dependent on the activation of PKC, p38 and JNK, and the synthesis of IL-1beta, TNF-alpha and IL-6 associated with the up-regulation of both B(1) and B(2) kinin receptors.
Signaling mediated by bradykinin B2 receptors contributes to mortality and secondary brain damage after subarachnoid hemorrhage in mice.
This gene encodes a receptor for bradykinin. The 9 aa bradykinin peptide elicits many responses including vasodilation, edema, smooth muscle spasm and pain fiber stimulation. This receptor associates with G proteins that stimulate a phosphatidylinositol-calcium second messenger system. Alternate start codons result in two isoforms of the protein.
B2 bradykinin receptor
, BK-2 receptor
, bradykinin B2 receptor
, ornithokinin receptor
, bradykinin receptor B2
, B2 bradykinin receptor-like
, b2 bradykinin receptor-like
, bradykinin receptor, beta 2
, kinin B2