Datasheet

生物学的記述

Specificity	Leptin Antibody (Mouse mAb) [D16P10] detects endogenous levels of total Leptin protein.
Background	Leptin is an adipocyte‑derived peptide hormone of the class I cytokine family that signals the status of peripheral energy stores to the brain, acting primarily through the long signaling isoform of its receptor (LepRb/Ob‑Rb) on hypothalamic and extra‑hypothalamic neurons to coordinate appetite, energy expenditure, and neuroendocrine function. The mature protein adopts a four‑helix bundle cytokine‑like structure that engages LepRb on target cells and promotes receptor dimerization, which brings associated JAK2 molecules into proximity and allows trans‑phosphorylation of JAK2 and tyrosine residues in the LepRb cytoplasmic tail; these phosphotyrosines then function as docking sites for STAT3, STAT5, and SHP2, initiating parallel JAK2–STAT, MAPK/ERK, and PI3K signaling cascades that modulate transcriptional programs controlling food intake, thermogenesis, glucose handling, and lipid metabolism. Within the arcuate nucleus, LepRb activation stimulates anorexigenic POMC/CART neurons and inhibits orexigenic NPY/AgRP neurons, leading to reduced appetite and increased sympathetic outflow to brown adipose tissue, while LepRb signaling in additional nuclei such as the ventromedial, dorsomedial, lateral hypothalamus, and preoptic area adjusts thermogenesis, heart rate, blood pressure, circadian feeding rhythms, and adaptive changes in energy expenditure during fasting or overnutrition. Leptin also acts as a permissive factor for reproductive and neuroendocrine axes, where adequate circulating leptin supports normal gonadotropin release, thyroid function, and adrenal activity, and leptin replacement in states of congenital or acquired leptin deficiency normalizes profound hypogonadism, thyroid suppression, and other neuroendocrine adaptations to chronic energy deficit in humans. On a cellular level, LepRb‑driven STAT3 signaling induces negative feedback regulators such as SOCS3 and protein tyrosine phosphatases, which attenuate JAK2 and receptor phosphorylation and contribute, together with impaired leptin transport across the blood–brain barrier and inflammatory/stress kinases, to central leptin resistance in common obesity, a state characterized by high circulating leptin but blunted hypothalamic responses and limited weight‑loss efficacy of exogenous leptin. Leptin signaling influences immune responses, bone metabolism, and cardiovascular function, with elevated leptin in obesity linked to hypertension, atherosclerosis, cardiac remodeling, and altered hematopoiesis, while physiological or pharmacological leptin repletion after weight loss partially reverses adaptive reductions in energy expenditure and hunger signals and is being explored as a tool for weight‑loss maintenance rather than primary weight reduction.

Specificity

Leptin Antibody (Mouse mAb) [D16P10] detects endogenous levels of total Leptin protein.

Background

Leptin is an adipocyte‑derived peptide hormone of the class I cytokine family that signals the status of peripheral energy stores to the brain, acting primarily through the long signaling isoform of its receptor (LepRb/Ob‑Rb) on hypothalamic and extra‑hypothalamic neurons to coordinate appetite, energy expenditure, and neuroendocrine function. The mature protein adopts a four‑helix bundle cytokine‑like structure that engages LepRb on target cells and promotes receptor dimerization, which brings associated JAK2 molecules into proximity and allows trans‑phosphorylation of JAK2 and tyrosine residues in the LepRb cytoplasmic tail; these phosphotyrosines then function as docking sites for STAT3, STAT5, and SHP2, initiating parallel JAK2–STAT, MAPK/ERK, and PI3K signaling cascades that modulate transcriptional programs controlling food intake, thermogenesis, glucose handling, and lipid metabolism. Within the arcuate nucleus, LepRb activation stimulates anorexigenic POMC/CART neurons and inhibits orexigenic NPY/AgRP neurons, leading to reduced appetite and increased sympathetic outflow to brown adipose tissue, while LepRb signaling in additional nuclei such as the ventromedial, dorsomedial, lateral hypothalamus, and preoptic area adjusts thermogenesis, heart rate, blood pressure, circadian feeding rhythms, and adaptive changes in energy expenditure during fasting or overnutrition. Leptin also acts as a permissive factor for reproductive and neuroendocrine axes, where adequate circulating leptin supports normal gonadotropin release, thyroid function, and adrenal activity, and leptin replacement in states of congenital or acquired leptin deficiency normalizes profound hypogonadism, thyroid suppression, and other neuroendocrine adaptations to chronic energy deficit in humans. On a cellular level, LepRb‑driven STAT3 signaling induces negative feedback regulators such as SOCS3 and protein tyrosine phosphatases, which attenuate JAK2 and receptor phosphorylation and contribute, together with impaired leptin transport across the blood–brain barrier and inflammatory/stress kinases, to central leptin resistance in common obesity, a state characterized by high circulating leptin but blunted hypothalamic responses and limited weight‑loss efficacy of exogenous leptin. Leptin signaling influences immune responses, bone metabolism, and cardiovascular function, with elevated leptin in obesity linked to hypertension, atherosclerosis, cardiac remodeling, and altered hematopoiesis, while physiological or pharmacological leptin repletion after weight loss partially reverses adaptive reductions in energy expenditure and hunger signals and is being explored as a tool for weight‑loss maintenance rather than primary weight reduction.

使用情報

Application

WB

Dilution

WB

1:1000

Reactivity

Human

Source

Mouse Monoclonal Antibody

MW

19 kDa

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

プロトコール

References

https://pubmed.ncbi.nlm.nih.gov/25343030/
https://pubmed.ncbi.nlm.nih.gov/38027481/

Leptin Antibody (Mouse mAb) [D16P10]

生物学的記述

使用情報

References

Application Data