Date published: 2026-2-14

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MRAP2 Activators

Chemical activators of MRAP2 include a range of hormones and peptides that engage in complex signaling pathways to upregulate the protein. ACTH (1-24), a fragment of adrenocorticotropic hormone, can stimulate the adrenal cortex to produce cortisol, which can lead to an upregulation of MRAP2 expression. This is a part of the body's response to stress, where MRAP2 plays a role in adrenal function. Similarly, Corticotropin-releasing hormone initiates a cascade by activating the hypothalamic-pituitary-adrenal (HPA) axis, resulting in increased production of ACTH from the pituitary and subsequent upregulation of MRAP2 in the adrenal gland.

Melanotan II, a synthetic analog of the naturally occurring melanocortin peptide, α-MSH, can activate melanocortin receptors, which are part of the pathway that regulates the expression of MRAP2. This activation can lead to an increase in MRAP2 expression as part of the signaling cascade involved in energy homeostasis. On the other hand, aldosterone, a mineralocorticoid hormone, can bind its receptors and affect gene transcription, which includes the upregulation of MRAP2. This is significant in the context of sodium retention and blood pressure regulation. Insulin, the central hormone in glucose metabolism, can upregulate MRAP2 expression by activating its receptor and initiating a series of intracellular signaling events that promote cellular uptake of glucose and metabolic regulation. Epinephrine and norepinephrine, both catecholamines, can also increase MRAP2 expression through their interactions with adrenergic receptors, which are pivotal in the fight or flight response, regulating processes such as heart rate and energy mobilization. Vasopressin, a peptide hormone known for its role in water retention and vasoconstriction, can activate V1a receptors, leading to a signaling pathway that results in the upregulation of MRAP2. This indicates MRAP2's role in fluid balance and cardiovascular system regulation. Thyrotropin-releasing hormone, which regulates the thyroid axis, can have an indirect effect on MRAP2 expression as part of the endocrine system's feedback loops. Lastly, human chorionic gonadotropin, a hormone associated with pregnancy and reproduction, can bind to its receptors and activate downstream signaling that includes the upregulation of MRAP2, signifying its role in steroidogenesis. Each of these chemicals, through their respective pathways, can engage MRAP2 in a way that leads to its functional activation, illustrating the protein's widespread involvement in various physiological processes.

SEE ALSO...

Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

Angiotensin II, Human

4474-91-3sc-363643
sc-363643A
sc-363643B
sc-363643C
1 mg
5 mg
25 mg
100 mg
$51.00
$100.00
$310.00
$690.00
3
(1)

Angiotensin II can increase the expression of MRAP2 through the activation of AT1 receptors and subsequent signaling pathways.

Aldosterone

52-39-1sc-210774
sc-210774A
sc-210774B
sc-210774C
sc-210774D
sc-210774E
2 mg
5 mg
10 mg
50 mg
100 mg
250 mg
$259.00
$213.00
$317.00
$1550.00
$3074.00
$7637.00
1
(1)

Aldosterone may upregulate MRAP2 expression by binding to mineralocorticoid receptors and influencing gene transcription.

Insulin

11061-68-0sc-29062
sc-29062A
sc-29062B
100 mg
1 g
10 g
$156.00
$1248.00
$12508.00
82
(1)

Insulin can enhance the expression of MRAP2 by activating insulin receptors and downstream signaling pathways.

(−)-Epinephrine

51-43-4sc-205674
sc-205674A
sc-205674B
sc-205674C
sc-205674D
1 g
5 g
10 g
100 g
1 kg
$41.00
$104.00
$201.00
$1774.00
$16500.00
(1)

Epinephrine can influence the expression of MRAP2 through adrenergic receptor activation and cAMP signaling pathways.

L-Noradrenaline

51-41-2sc-357366
sc-357366A
1 g
5 g
$326.00
$485.00
3
(0)

Norepinephrine can stimulate the expression of MRAP2 via adrenergic receptors and their associated signaling cascades.

Vasopressin

11000-17-2sc-356188
sc-356188A
5 mg
25 mg
$260.00
$1040.00
1
(0)

Vasopressin may increase MRAP2 expression through V1a receptor activation and subsequent second messenger pathways.