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Leptin Receptor (LEPR) Antibody (N-term)
Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| IHC-P, WB, FC, E |
|---|---|
| Primary Accession | P48357 |
| Other Accession | NP_002294 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 132494 Da |
| Antigen Region | 23-52 aa |
| Gene ID | 3953 |
|---|---|
| Other Names | Leptin receptor, LEP-R, HuB219, OB receptor, OB-R, CD295, LEPR, DB, OBR |
| Target/Specificity | This Leptin Receptor (LEPR) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 23-52 amino acids from the N-terminal region of human Leptin Receptor (LEPR). |
| Dilution | WB~~1:1000 IHC-P~~1:50~100 FC~~1:10~50 |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | Leptin Receptor (LEPR) Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | LEPR |
|---|---|
| Synonyms | DB, OBR |
| Function | Receptor for hormone LEP/leptin (Probable) (PubMed:22405007). On ligand binding, mediates LEP central and peripheral effects through the activation of different signaling pathways such as JAK2/STAT3 and MAPK cascade/FOS. In the hypothalamus, LEP acts as an appetite- regulating factor that induces a decrease in food intake and an increase in energy consumption by inducing anorexinogenic factors and suppressing orexigenic neuropeptides, also regulates bone mass and secretion of hypothalamo-pituitary-adrenal hormones (By similarity) (PubMed:9537324). In the periphery, increases basal metabolism, influences reproductive function, regulates pancreatic beta-cell function and insulin secretion, is pro-angiogenic and affects innate and adaptive immunity (PubMed:25060689, PubMed:12504075, PubMed:8805376). Control of energy homeostasis and melanocortin production (stimulation of POMC and full repression of AgRP transcription) is mediated by STAT3 signaling, whereas distinct signals regulate NPY and the control of fertility, growth and glucose homeostasis. Involved in the regulation of counter-regulatory response to hypoglycemia by inhibiting neurons of the parabrachial nucleus. Has a specific effect on T lymphocyte responses, differentially regulating the proliferation of naive and memory T -ells. Leptin increases Th1 and suppresses Th2 cytokine production (By similarity). |
| Cellular Location | Cell membrane; Single-pass type I membrane protein. Basolateral cell membrane |
| Tissue Location | Isoform A is expressed in fetal liver and in hematopoietic tissues and choroid plexus. In adults highest expression in heart, liver, small intestine, prostate and ovary. Low level in lung and kidney. Isoform B is highly expressed in hypothalamus, but also in skeletal muscle. Detected in fundic and antral epithelial cells of the gastric mucosa (PubMed:19159218). Isoform B and isoform A are expressed by NK cells (at protein level) (PubMed:12504075) |
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Provided below are standard protocols that you may find useful for product applications.
Background
Leptin, an adipocyte-specific hormone, regulates adipose-tissue mass through hypothalamic effects on satiety and energy expenditure by acting through the leptin receptor (LEPR). LEPR is a single-transmembrane-domain receptor of the cytokine receptor family that is identical to the mouse diabetes (db) gene product. During weight loss, leptin levels decrease, whereas soluble LEPR levels and the receptor bound fraction of leptin increases. The presence of LEPR in the absorptive cells of the small intestine suggests that leptin may have a physiological role in the regulation of nutrient absorption.
References
Schroth, M., et al., J. Clin. Endocrinol. Metab. 88(11):5497-5501 (2003).
Couturier, C., et al., J. Biol. Chem. 278(29):26604-26611 (2003).
Gavrila, A., et al., J. Clin. Endocrinol. Metab. 88(6):2838-2843 (2003).
Yannakoulia, M., et al., J. Clin. Endocrinol. Metab. 88(4):1730-1736 (2003).
Kado, N., et al., Hum. Reprod. 18(4):715-720 (2003).
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