Ghrelin Antibody [F2E5] | Primary Antibodies

Application: Reactivity: Mouse, Rat, Human

Usage Information

Dilution
IHC1:8000

Application
IHC

Reactivity
Mouse, Rat, Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Datasheet & SDS

Biological Description

Specificity
Ghrelin Antibody [F2E5] detects endogenous levels of total Ghrelin protein.

Clone
F2E5

Synonym(s)
MTLRP; UNQ524/PRO1066; GHRL; Appetite‑regulating hormone; Growth hormone secretagogue; Growth hormone‑releasing peptide; Motilin‑related peptide; Protein M46

Background
Ghrelin is an acylated peptide hormone synthesized predominantly in gastric enteroendocrine cells, with additional expression in the pancreas, lung, and hypothalamic neurons, where it acts as a key peripheral and central regulator of energy homeostasis, growth hormone release, and reward related feeding behavior. The mature ligand binds to the growth hormone secretagogue receptor (GHSR/GHS R1a), a class A G protein–coupled receptor highly expressed in the hypothalamic arcuate nucleus, pituitary, and midbrain dopamine circuits, engaging multiple G protein families including Gαq/11, Gαi/o, and Gα12/13, which activate phospholipase C–inositol trisphosphate–calcium signaling, inhibit adenylate cyclase, and recruit Rho A–dependent pathways, respectively, while β arrestins additionally mediate GHSR internalization and MAPK activation. In the arcuate nucleus, ghrelin GHSR signaling stimulates neuropeptide Y and agouti related peptide–expressing orexigenic neurons, increases AMP activated protein kinase activity, and disinhibits dopaminergic reward pathways, thereby promoting hunger, anticipatory feeding, and preference for calorie dense foods, whereas in the pituitary the same receptor ligand pair drives calcium dependent growth hormone secretion, linking ghrelin to somatotropic axis control and metabolic adaptation. Ghrelin also modulates gastric motility, acid secretion, and pancreatic islet function. Ghrelin-mediated Gαi signalling attenuates glucose-stimulated insulin release, thereby coordinating energy intake, storage, and fuel utilisation under fasted states. In contrast, its circulating levels normally decline after meals to disinhibit satiety pathways governed by leptin and insulin. In obesity, ghrelin suppression can blunt meal-induced inhibition of appetite and impair metabolic flexibility. Conversely, in cachexia and chronic illness, reduced ghrelin tone may exacerbate negative energy balance and muscle wasting, ultimately leading to dysregulated ghrelin-GHSR signalling across both hyperphagic and catabolic metabolic states.

Background

Ghrelin is an acylated peptide hormone synthesized predominantly in gastric enteroendocrine cells, with additional expression in the pancreas, lung, and hypothalamic neurons, where it acts as a key peripheral and central regulator of energy homeostasis, growth hormone release, and reward related feeding behavior. The mature ligand binds to the growth hormone secretagogue receptor (GHSR/GHS R1a), a class A G protein–coupled receptor highly expressed in the hypothalamic arcuate nucleus, pituitary, and midbrain dopamine circuits, engaging multiple G protein families including Gαq/11, Gαi/o, and Gα12/13, which activate phospholipase C–inositol trisphosphate–calcium signaling, inhibit adenylate cyclase, and recruit Rho A–dependent pathways, respectively, while β arrestins additionally mediate GHSR internalization and MAPK activation. In the arcuate nucleus, ghrelin GHSR signaling stimulates neuropeptide Y and agouti related peptide–expressing orexigenic neurons, increases AMP activated protein kinase activity, and disinhibits dopaminergic reward pathways, thereby promoting hunger, anticipatory feeding, and preference for calorie dense foods, whereas in the pituitary the same receptor ligand pair drives calcium dependent growth hormone secretion, linking ghrelin to somatotropic axis control and metabolic adaptation. Ghrelin also modulates gastric motility, acid secretion, and pancreatic islet function. Ghrelin-mediated Gαi signalling attenuates glucose-stimulated insulin release, thereby coordinating energy intake, storage, and fuel utilisation under fasted states. In contrast, its circulating levels normally decline after meals to disinhibit satiety pathways governed by leptin and insulin. In obesity, ghrelin suppression can blunt meal-induced inhibition of appetite and impair metabolic flexibility. Conversely, in cachexia and chronic illness, reduced ghrelin tone may exacerbate negative energy balance and muscle wasting, ultimately leading to dysregulated ghrelin-GHSR signalling across both hyperphagic and catabolic metabolic states.

References
https://pubmed.ncbi.nlm.nih.gov/22249814/ https://pubmed.ncbi.nlm.nih.gov/30177523/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%