Use your antibodies-online credentials, if available.
Intermedin binds the RAMP1/CLR complex via a triple beta-turn.
Study revealed that exogenous intermedin up-regulates the expression of VEGF and RAMP2 at least partially via activating Wnt/beta-catenin signaling, finally promoting angiogenesis of hypoxia and reoxygenation impaired HUVECs in vitro.
IMD may be an important self-protective factor in response to sepsis.
The plasma ADM2 levels were inversely correlated with obesity in humans, and adipo-ADM2-transgenic (tg) mice displayed resistance to high-fat diet-induced obesity with increased energy expenditure.
Mouse and human heart valves expressed mRNAs for the CRL ligands adrenomedullin (AM), adrenomedullin-2 (AM-2) and calcitonin gene-related peptide (CGRP) and for their receptor components, i.e., CRL and receptor-activity-modifying proteins 1-3.
ADM-2 is a stress-inducible gene controlled by ATF-4.
Intermedin1-53 may attenuate vascular calcification by upregulating alpha-Klotho via the calcitonin receptor/modifying protein complex and protein kinase A signaling.
Intermedin (IMD) derived from human cardiac microvascular endothelial cell and acting in a paracrine manner on cardiomyocytes, predominantly at AM1 receptors, is more likely to contribute to direct protection by endogenous IMD of cardiomyocytes against acute ischemia reperfusion injury.
Elevated plasma intermedin levels are independently associated with long-term recurrence and distant metastasis of prostate cancer.
ADM2 may contribute to the physiology of embryo implantation and placental growth via increasing MMP2 and decreasing MUC1 expression to facilitate trophoblast invasion.
Plasma intermedin and BNP levels were markedly higher in acute coronary syndrome patients than in healthy people.
High levels of ADM2 expression predict a poorer survival in patients with pancreatic adenocarcinoma.
TSH induced AM2/IMD expression in the thyroid gland and it could locally work as a potent vasodilator, resulting in the expansion of thyroid inter-follicular capillaries.
Intermedin affects the endothelial cell junction and blood vessel sprouting in a VE-cadherin dependent way.
results suggest that high plasma intermedin level is associated with poor outcomes of patients and may be a useful prognostic biomarker in ST-segment elevation acute myocardial infarction.
ADM and IMD mRNA expression are elevated in chronic heart failure at different stages of the disease.
a significant increase in plasma intermedin following acute myocardial infarction may be associated with oxidative stress, and could be used as a marker to reflect the severity of the coronary stenosis
this study is the first to demonstrate a potential involvement of IMD in human embryo implantation and placental development via regulation of trophoblast invasion at the maternal-fetal interface
Intermedin plays a critical role in the vascular remodeling process and tumor angiogenesis by regulating vascular endothelial-cadherin and extracellular signal-regulated kinase.
adm2 polymorphism is associated with renal dysfunction, blood pressure regulation and asymptomatic cerebrovascular diseases in the Japanese general population
Quiescent endothelial cells overcome contact inhibition and regain the ability to proliferate for continuous vascular lumen enlargement via intermedin signaling.
Intermedin attenuated neointima formation in the mouse model of common carotid-artery ligation injury. IMD protection may be mediated by maintaining a vascular smooth muscle cell contractile phenotype via the cAMP/PKA pathway.
results indicate that endogenous AM2 might be involved in energy metabolism in adipocytes through the upregulation of UCP1 expression
ADM2 enhances subcutaneous White Adipose Tissue beiging via a direct effect by activating the CRLR.RAMP1-cAMP/PKA and p38 MAPK pathways in white adipocytes and via an indirect effect by stimulating alternative M2 polarization in macrophages.
IMD reduces bone resorption by inhibiting osteoblast apoptosis, decreasing the RANKL/OPG ratio and the expression of M-CSF, and inhibiting osteoclast maturation and differentiation.
Adrenomedullin-2/intermedin(8-47) ameliorates early ischemia/reperfusion injury in mouse lungs by protecting the integrity of the blood-air barrier and by potently reducing leukocyte influx into the alveolar space
Intermedin attenuates macrophage foam-cell formation via tristetraprolin-mediated degradation of CD36 mRNA.
increased stability of PTEN by intermedin leads to SR-A inhibition in macrophages, which ameliorates foam-cell formation and atherosclerosis in apoE(-/-) mice.
Data show that mechanical ventilation reduced the expression of receptor activity-modifying protein RAMP3, but not of intermedin (IMD), calcitonin receptor-like receptor (CRLR), and RAMP1 and RAMP2.
Intermedin is a calcitonin/calcitonin gene-related peptide family peptide acting through the calcitonin receptor-like receptor/receptor activity-modifying protein receptor complexes
Our data suggest that IMD acutely augments cardiomyocyte contractile function through, at least in part, a protein kinase C- and protein kinase A-dependent mechanism.
tissue adrenomedullin 2 intermedin content was positively correlated with the diastolic blood pressure and negatively correlated with pulse pressure
IMD is a novel hypoxia-induced gene and a potential interventional agent for the improvement of endothelial barrier function in systemic inflammatory responses and hypoxia-induced vascular leakage.
This gene encodes a protein which is a member of the calcitonin-related hormones. The encoded protein is involved in maintaining homeostasis in many tissues, acting via CRLR/RAMP receptor (calcitonin receptor-like receptor/receptor activity-modifying protein) complexes. Multiple alternatively spliced variants, encoding the same protein, have been identified.
, adrenomedullin 2 precusor