Orexin A Antibody (Rabbit mAb) [P6H3]

Application: Reactivity: Mouse, Rat

Usage Information

Dilution
IHC1:1000

Application
IHC, ELISA

Reactivity
Mouse, Rat

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

Predicted MW
13 kDa

Positive Control	Mouse hypothalamus tissue; Rat hypothalamus tissue
Negative Control

Datasheet & SDS

Biological Description

Specificity
Orexin A Antibody (Rabbit mAb) [P6H3] detects endogenous levels of total Orexin A peptide.

Clone
P6H3

Synonym(s)
Ox, Ppox, Hcrt, Hypocretin neuropeptide precursor, Hypocretin, Orexin precursor, Prepro-orexin, Preprohypocretin

Background
Orexin A, together with orexin B, is one of two neuropeptides derived by proteolytic cleavage from a single prepro-orexin precursor, synthesized exclusively by neurons localized within the lateral and posterior hypothalamus. Both peptides bind and activate two closely related G protein-coupled receptors, OX1R and OX2R, with orexin A engaging both receptor subtypes with comparable affinity, while orexin B shows selectivity favoring OX2R, giving the two-peptide, two-receptor system built-in signaling diversity. Orexin neurons project extensively throughout the central nervous system, including to major nuclei governing sleep-wake regulation, and central administration of orexin A directly stimulates food consumption, linking hypothalamic orexin signaling to acute feeding behavior. Prepro-orexin mRNA expression rises during fasting, positioning the orexin system as a feedback mediator that couples nutritional state to feeding drive rather than acting as a constitutively active signal. Orexin neurons are directly regulated by circulating glucose, leptin, and ghrelin, and this responsiveness allows the orexin system to adjust arousal output according to whole-body energy balance, increasing wakefulness during states of energy deficit such as fasting. OX2R signaling is the primary driver of sleep-wake state stabilization, with receptor activity in the tuberomammillary nucleus and basal forebrain regions maintaining wakefulness, while OX1R signaling contributes additionally to reward-related and motivated behaviors through projections to mesolimbic circuits. Genetic loss of orexin neurons or disruption of OX2R signaling produces a phenotype of poor wakefulness maintenance and cataplexy that closely mirrors human narcolepsy, and this loss-of-function relationship has directly informed the development of OX2R-selective agonists as a therapeutic strategy targeting the underlying neurochemical deficit in narcolepsy type 1, distinct from orexin receptor antagonists developed for insomnia by blocking the same wake-promoting pathway.

Background

Orexin A, together with orexin B, is one of two neuropeptides derived by proteolytic cleavage from a single prepro-orexin precursor, synthesized exclusively by neurons localized within the lateral and posterior hypothalamus. Both peptides bind and activate two closely related G protein-coupled receptors, OX1R and OX2R, with orexin A engaging both receptor subtypes with comparable affinity, while orexin B shows selectivity favoring OX2R, giving the two-peptide, two-receptor system built-in signaling diversity. Orexin neurons project extensively throughout the central nervous system, including to major nuclei governing sleep-wake regulation, and central administration of orexin A directly stimulates food consumption, linking hypothalamic orexin signaling to acute feeding behavior. Prepro-orexin mRNA expression rises during fasting, positioning the orexin system as a feedback mediator that couples nutritional state to feeding drive rather than acting as a constitutively active signal. Orexin neurons are directly regulated by circulating glucose, leptin, and ghrelin, and this responsiveness allows the orexin system to adjust arousal output according to whole-body energy balance, increasing wakefulness during states of energy deficit such as fasting. OX2R signaling is the primary driver of sleep-wake state stabilization, with receptor activity in the tuberomammillary nucleus and basal forebrain regions maintaining wakefulness, while OX1R signaling contributes additionally to reward-related and motivated behaviors through projections to mesolimbic circuits. Genetic loss of orexin neurons or disruption of OX2R signaling produces a phenotype of poor wakefulness maintenance and cataplexy that closely mirrors human narcolepsy, and this loss-of-function relationship has directly informed the development of OX2R-selective agonists as a therapeutic strategy targeting the underlying neurochemical deficit in narcolepsy type 1, distinct from orexin receptor antagonists developed for insomnia by blocking the same wake-promoting pathway.

References
https://pubmed.ncbi.nlm.nih.gov/9491897/ https://www.nature.com/articles/nrn2092

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%