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ADM-2 is a stress-inducible gene controlled by ATF-4 (show ATF4 ELISA Kits).
Intermedin1-53 may attenuate vascular calcification by upregulating alpha-Klotho (show KL ELISA Kits) via the calcitonin receptor (show CALCR ELISA Kits)/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 (show MMP2 ELISA Kits) and decreasing MUC1 (show MUC1 ELISA Kits) 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 (show CDH5 ELISA Kits) 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.
IMD reduces bone resorption by inhibiting osteoblast apoptosis, decreasing the RANKL/OPG (show TNFSF11 ELISA Kits) ratio and the expression of M-CSF (show CSF1R ELISA Kits), 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 (show ZFP36 ELISA Kits)-mediated degradation of CD36 (show CD36 ELISA Kits) mRNA.
increased stability of PTEN by intermedin leads to SR-A (show MSR1 ELISA Kits) inhibition in macrophages, which ameliorates foam-cell formation and atherosclerosis in apoE (show APOE ELISA Kits)(-/-) mice.
Data show that mechanical ventilation reduced the expression of receptor activity-modifying protein RAMP3 (show RAMP3 ELISA Kits), but not of intermedin (IMD), calcitonin receptor-like receptor (CRLR (show CALCRL ELISA Kits)), and RAMP1 (show RAMP1 ELISA Kits) and RAMP2 (show RAMP2 ELISA Kits).
Intermedin is a calcitonin/calcitonin (show CALCA ELISA Kits) gene-related peptide (show CALCA ELISA Kits) family peptide acting through the calcitonin receptor-like receptor (show CALCRL ELISA Kits)/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 (show PKC ELISA Kits)- 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