Target intelligence / Profile preview

Allatotropin receptor (ATR)

Target
ATR
Molecular classification
G protein-coupled receptor, Neuropeptide receptor
01

Overview

Allatotropin is a neuropeptide first characterized in insects for its role in stimulating the biosynthesis of juvenile hormone, a master regulator of insect growth, metamorphosis, and reproduction[1][3][5][7][9]. Allatotropins are found in a wide range of invertebrates including insects, mollusks, flatworms, and some annelids, suggesting ancient evolutionary conservation[1][2][6][7]. The Allatotropin receptor (ATR) is a G protein-coupled receptor expressed in target tissues such as the corpora allata, accessory glands, heart, gut, and reproductive organs[3][4][5]. Activation of this receptor triggers intracellular signaling cascades that regulate hormone synthesis, muscle contractions, cardiac rhythm, digestive enzyme secretion, and reproductive physiology[2][3][4][5][6][7]. Allatotropin signaling is pivotal in insect biology but does not have a known role in human physiology or disease. No clinical drugs or biomarkers are associated with Allatotropin or its receptor. The process termed "Allatotropins secretion" refers to the physiological process of Allatotropin peptide release and does not denote a molecular target. The scientifically accurate target for structured database use is the Allatotropin receptor (ATR).

Other names
Allatotropin receptorATRAT receptorAeATr
02

Mechanism of action

Activation of Allatotropin receptor by Allatotropin triggers G protein signaling (primarily Gq/PLC/IP3/Ca2+ or Gs/cAMP pathways). Stimulation modulates downstream physiological effects: juvenile hormone synthesis, muscle contraction, secretion.

03

Biological functions

Signal transductionMyoregulationStimulation of juvenile hormone biosynthesisCardiac rhythm modulationRegulation of digestive enzyme secretionControl of reproductive physiology
04

Disease associations

Other
05

Safety considerations

Not applicable
06

Interacting drugs

None
07

Biomarkers

None

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