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The plasma ADM2 levels were inversely correlated with obesity in humans, and adipo-ADM2-transgenic (tg) mice displayed resista (Montrer MAPK14 Protéines)nce to high-fat diet-induced obesity with increased energy expenditure.
Mouse and human heart valves expressed mRNAs for the CRL (Montrer IL31RA Protéines) ligands adrenomedullin (Montrer ADM Protéines) (AM), adrenomedullin-2 (AM-2) and calcitonin gene-related peptide (CGRP (Montrer CALCA Protéines)) and for their receptor components, i.e., CRL (Montrer IL31RA Protéines) and receptor-activity-modifying proteins 1-3.
ADM-2 is a stress-inducible gene controlled by ATF-4 (Montrer ATF4 Protéines).
Intermedin1-53 may attenuate vascular calcification by upregulating alpha-Klotho (Montrer KL Protéines) via the calcitonin receptor (Montrer CALCR Protéines)/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 (Montrer MMP2 Protéines) and decreasing MUC1 (Montrer MUC1 Protéines) 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.
results indicate that endogenous AM2 might be involved in energy metabolism in adipocytes through the upregulation of UCP1 (Montrer UCP1 Protéines) expression
ADM2 enhances subcutaneous White Adipose Tissue beiging via a direct effect by activating the CRLR.RAMP1-cAMP/PKA and p38 MAPK (Montrer MAPK14 Protéines) pathways in white adipocytes and via an indirect effect by stimulating alternative M2 polarization in macrophages.
Mouse and human heart valves expressed mRNAs for the CRL ligands adrenomedullin (Montrer ADM Protéines) (AM), adrenomedullin-2 (AM-2) and calcitonin gene-related peptide (CGRP (Montrer CALCA Protéines)) and for their receptor components, i.e., CRL and receptor-activity-modifying proteins 1-3.
IMD reduces bone resorption by inhibiting osteoblast apoptosis, decreasing the RANKL/OPG (Montrer TNFSF11 Protéines) ratio and the expression of M-CSF (Montrer CSF1R Protéines), 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 (Montrer ZFP36 Protéines)-mediated degradation of CD36 (Montrer CD36 Protéines) mRNA.
increased stability of PTEN by intermedin leads to SR-A (Montrer MSR1 Protéines) inhibition in macrophages, which ameliorates foam-cell formation and atherosclerosis in apoE (Montrer APOE Protéines)(-/-) mice.
Data show that mechanical ventilation reduced the expression of receptor activity-modifying protein RAMP3 (Montrer RAMP3 Protéines), but not of intermedin (IMD), calcitonin receptor-like receptor (CRLR (Montrer CALCRL Protéines)), and RAMP1 (Montrer RAMP1 Protéines) and RAMP2 (Montrer RAMP2 Protéines).
Intermedin is a calcitonin/calcitonin (Montrer CALCA Protéines) gene-related peptide (Montrer CALCA Protéines) family peptide acting through the calcitonin receptor-like receptor (Montrer CALCRL Protéines)/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.
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