Name: Anti-Glucocorticoid Receptor alpha antibody
SKU: ab3580
Rating: 3 (3 reviews)

Rabbit Polyclonal Glucocorticoid Receptor antibody. Suitable for IHC-P, ICC/IF and reacts with Human samples. Cited in 32 publications. Immunogen corresponding to Synthetic Peptide within Human NR3C1 aa 750 to C-terminus.

Images

Immunocytochemistry/ Immunofluorescence - Anti-Glucocorticoid Receptor alpha antibody (AB3580), expandable thumbnail

Publications

Key facts

Isotype: IgG
Host species: Rabbit
Storage buffer: Preservative: 0.05% Sodium azide
Constituents: 99% PBS
Form: Liquid
Clonality: Polyclonal

Immunogen

Synthetic Peptide within Human NR3C1 aa 750 to C-terminus. The exact immunogen used to generate this antibody is proprietary information. Database link P04150

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Reactivity data

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Product promiseTestedExpectedPredictedNot recommended

	IHC-P	ICC/IF
Human	Tested	Tested

Tested
Tested

Species	Dilution info	Notes
Species Human	Dilution info 1/20	Notes -

Tested
Tested

Species	Dilution info	Notes
Species Human	Dilution info 1/100.00000 - 1/200.00000	Notes -

Target data

See full target information NR3C1

Function

Receptor for glucocorticoids (GC) (PubMed:27120390, PubMed:37478846). Has a dual mode of action: as a transcription factor that binds to glucocorticoid response elements (GRE), both for nuclear and mitochondrial DNA, and as a modulator of other transcription factors (PubMed:28139699). Affects inflammatory responses, cellular proliferation and differentiation in target tissues. Involved in chromatin remodeling (PubMed:9590696). Plays a role in rapid mRNA degradation by binding to the 5' UTR of target mRNAs and interacting with PNRC2 in a ligand-dependent manner which recruits the RNA helicase UPF1 and the mRNA-decapping enzyme DCP1A, leading to RNA decay (PubMed:25775514). Could act as a coactivator for STAT5-dependent transcription upon growth hormone (GH) stimulation and could reveal an essential role of hepatic GR in the control of body growth (By similarity). Isoform Alpha. Has transcriptional activation and repression activity (PubMed:11435610, PubMed:15769988, PubMed:15866175, PubMed:17635946, PubMed:19141540, PubMed:19248771, PubMed:20484466, PubMed:21664385, PubMed:23820903). Mediates glucocorticoid-induced apoptosis (PubMed:23303127). Promotes accurate chromosome segregation during mitosis (PubMed:25847991). May act as a tumor suppressor (PubMed:25847991). May play a negative role in adipogenesis through the regulation of lipolytic and antilipogenic gene expression (By similarity). Isoform Beta. Acts as a dominant negative inhibitor of isoform Alpha (PubMed:20484466, PubMed:7769088, PubMed:8621628). Has intrinsic transcriptional activity independent of isoform Alpha when both isoforms are coexpressed (PubMed:19248771, PubMed:26711253). Loses this transcription modulator function on its own (PubMed:20484466). Has no hormone-binding activity (PubMed:8621628). May play a role in controlling glucose metabolism by maintaining insulin sensitivity (By similarity). Reduces hepatic gluconeogenesis through down-regulation of PEPCK in an isoform Alpha-dependent manner (PubMed:26711253). Directly regulates STAT1 expression in isoform Alpha-independent manner (PubMed:26711253). Isoform Alpha-2. Has lower transcriptional activation activity than isoform Alpha. Exerts a dominant negative effect on isoform Alpha trans-repression mechanism (PubMed:20484466). Isoform GR-P. Increases activity of isoform Alpha. Isoform Alpha-B. More effective than isoform Alpha in transcriptional activation, but not repression activity. Isoform 10. Has transcriptional activation activity. Isoform Alpha-C1. Has transcriptional activation activity. Isoform Alpha-C2. Has transcriptional activation activity. Isoform Alpha-C3. Has highest transcriptional activation activity of all isoforms created by alternative initiation (PubMed:15866175, PubMed:23820903). Has transcriptional repression activity (PubMed:23303127). Mediates glucocorticoid-induced apoptosis (PubMed:23303127, PubMed:23820903). Isoform Alpha-D1. Has transcriptional activation activity. Isoform Alpha-D2. Has transcriptional activation activity. Isoform Alpha-D3. Has lowest transcriptional activation activity of all isoforms created by alternative initiation (PubMed:15866175, PubMed:23820903). Has transcriptional repression activity (PubMed:23303127).

Alternative names

GRL, NR3C1, Glucocorticoid receptor, GR, Nuclear receptor subfamily 3 group C member 1

Key facts

Isotype: IgG
Host species: Rabbit
Storage buffer: Preservative: 0.05% Sodium azide
Constituents: 99% PBS
Form: Liquid
Clonality: Polyclonal
Immunogen: Synthetic Peptide within Human NR3C1 aa 750 to C-terminus. The exact immunogen used to generate this antibody is proprietary information. Database link P04150
Purification technique: Affinity purification Immunogen
Concentration

Storage

Shipped at conditions: Blue Ice
Appropriate short-term storage duration: 1-2 weeks
Appropriate short-term storage conditions: +4°C
Appropriate long-term storage conditions: -20°C
Aliquoting information: Upon delivery aliquot
Storage information: Avoid freeze / thaw cycle

Notes

GR alpha proteins has many isoforms e.g. GR alpha-A, Alpha-2, GR-A alpha, Alpha-B. Please check Uniprot database or PMID 15866175 for more information.

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Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

The Glucocorticoid Receptor alpha also known as GR-alpha is a fundamental component in the family of nuclear receptors. It weighs approximately 97 kDa. This receptor is widely expressed in various tissues including the liver immune cells and the brain. The receptor functions through ligand-induced activation where it binds glucocorticoids. Upon binding GR-alpha undergoes a conformational change enabling it to translocate into the nucleus where it interacts with specific DNA sequences.

Biological function summary

The Glucocorticoid Receptor alpha influences numerous cellular processes like metabolism immune response and cell proliferation. It often functions as a part of larger protein complexes including transcriptional machinery. GR-alpha regulates gene expression by binding to glucocorticoid response elements (GRE) on DNA impacting the synthesis of specific proteins. This receptor modulates both positive and negative transcriptional control affecting various genes involved in biological responses.

Pathways

GR-alpha plays an important role in the Hypothalamic-Pituitary-Adrenal (HPA) axis and the inflammatory response pathway. In the HPA axis GR-alpha regulates cortisol synthesis and secretion impacting stress response and maintaining homeostasis. Within the inflammatory response GR-alpha interacts with NF-kB a protein complex that controls transcription of DNA to inhibit pro-inflammatory gene expression. These interactions exemplify GR-alpha’s regulatory influence on inflammation and stress-related responses.

Associated diseases and disorders

GR-alpha is implicated in various conditions such as Cushing's syndrome and rheumatoid arthritis. In Cushing's syndrome impaired function or expression of GR-alpha leads to uncontrolled cortisol levels resulting in multiple metabolic and physiological disturbances. In rheumatoid arthritis GR-alpha mediates anti-inflammatory effects which are important for disease management. Connections between GR-alpha and pro-inflammatory cytokines emphasize its role in modulating inflammatory responses in these diseases.

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9 product images

Immunocytochemistry/ Immunofluorescence - Anti-Glucocorticoid Receptor alpha antibody (ab3580)
Immunocytochemistry/Immunofluorescence analysis of U-251 MG (Human brain glioma cell line) cells labeling Glucocorticoid Receptor alpha (green) with ab3580 at 1/100. F-Actin staining with Phalloidin (red) and nuclei with DAPI (blue). Cells were fixed with formaldehyde and incubated with the primary antibody overnight at 4°C. A DyLight 488-conjugated secondary antibody was used. 60X magnification. Right - negative control.
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Glucocorticoid Receptor alpha antibody (ab3580)
Immunohistochemistry was performed on both normal and cancer biopsies of deparaffinized human tonsil tissue tissues. To expose target proteins heat induced antigen retrieval was performed using 10mM sodium citrate (pH6.0) buffer microwaved for 8-15 minutes. Following antigen retrieval tissues were blocked in 3% BSA-PBS for 30 minutes at room temperature. Tissues were then probed at a dilution of 1:50 with a rabbit polyclonal antibody recognizing Glucocorticoid Receptor alpha ab3580 or without primary antibody (negative control) overnight at 4°C in a humidified chamber. Tissues were washed extensively with PBST and endogenous peroxidase activity was quenched with a peroxidase suppressor. Detection was performed using a biotin-conjugated secondary antibody and SA-HRP followed by colorimetric detection using DAB. Tissues were counterstained with hematoxylin and prepped for mounting.
Immunocytochemistry/ Immunofluorescence - Anti-Glucocorticoid Receptor alpha antibody (ab3580)
Immunocytochemistry/Immunofluorescence analysis of HeLa (Human epithelial adenocarcinoma cell line) cells labeling Glucocorticoid Receptor alpha (green) with ab3580 at 1/100. F-Actin staining with Phalloidin (red) and nuclei with DAPI (blue). Cells were fixed with formaldehyde and incubated with the primary antibody overnight at 4°C. A DyLight 488-conjugated secondary antibody was used. 60X magnification. Right - negative control.
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Glucocorticoid Receptor alpha antibody (ab3580)
Immunohistochemistry was performed on both normal and cancer biopsies of deparaffinized human cervical carcinoma tissues. To expose target proteins heat induced antigen retrieval was performed using 10mM sodium citrate (pH6.0) buffer microwaved for 8-15 minutes. Following antigen retrieval tissues were blocked in 3% BSA-PBS for 30 minutes at room temperature. Tissues were then probed at a dilution of 1:20 with a rabbit polyclonal antibody recognizing Glucocorticoid Receptor alpha ab3580 or without primary antibody (negative control) overnight at 4°C in a humidified chamber. Tissues were washed extensively with PBST and endogenous peroxidase activity was quenched with a peroxidase suppressor. Detection was performed using a biotin-conjugated secondary antibody and SA-HRP followed by colorimetric detection using DAB. Tissues were counterstained with hematoxylin and prepped for mounting.
Immunocytochemistry/ Immunofluorescence - Anti-Glucocorticoid Receptor alpha antibody (ab3580)
Immunocytochemistry/Immunofluorescence analysis of A2058 (Human metastatic melanoma cell line) cells labeling Glucocorticoid Receptor alpha (green) with ab3580 at 1/200. F-Actin staining with Phalloidin (red) and nuclei with DAPI (blue). Cells were fixed with formaldehyde and incubated with the primary antibody overnight at 4°C. A DyLight 488-conjugated secondary antibody was used. 60X magnification. Right - negative control.
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Glucocorticoid Receptor alpha antibody (ab3580)
Immunohistochemistry was performed on both normal and cancer biopsies of deparaffinized human heart tissue tissues. To expose target proteins heat induced antigen retrieval was performed using 10mM sodium citrate (pH6.0) buffer microwaved for 8-15 minutes. Following antigen retrieval tissues were blocked in 3% BSA-PBS for 30 minutes at room temperature. Tissues were then probed at a dilution of 1:100 with a rabbit polyclonal antibody recognizing Glucocorticoid Receptor alpha ab3580 or without primary antibody (negative control) overnight at 4°C in a humidified chamber. Tissues were washed extensively with PBST and endogenous peroxidase activity was quenched with a peroxidase suppressor. Detection was performed using a biotin-conjugated secondary antibody and SA-HRP followed by colorimetric detection using DAB. Tissues were counterstained with hematoxylin and prepped for mounting.
Immunocytochemistry/ Immunofluorescence - Anti-Glucocorticoid Receptor alpha antibody (ab3580)
ab3580 staining glucocorticoid receptor in serum starved HeLa (Human epithelial adenocarcinoma cell line) cells treated with rosiglitazone (Rosiglitazone, PPARgamma agonist ab120762), by ICC/IF. Changes in localization of glucocorticoid receptor (translocation from cytoplasm to nucleous) correlates with increased concentration of rosiglitazone, as described in literature.
The cells were incubated at 37°C for 1h in media containing different concentrations of Rosiglitazone, PPARgamma agonist ab120762 (rosiglitazone) in DMSO, fixed with 4% formaldehyde for 10 minutes at room temperature and blocked with PBS containing 10% goat serum, 0.3 M glycine, 1% BSA and 0.1% tween for 2h at room temperature. Staining of the treated cells with ab3580 (5 μg/ml) was performed overnight at 4°C in PBS containing 1% BSA and 0.1% tween. A DyLight 488 goat anti-rabbit polyclonal antibody (Goat Anti-Rabbit IgG H&L (DyLight® 488) preadsorbed ab96899) at 1/250 dilution was used as the secondary antibody. Nuclei were counterstained with DAPI and are shown in blue.
This image is courtesy of an anonymous customer review
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Glucocorticoid Receptor alpha antibody (ab3580)
ab3580 staining Glucocorticoid Receptor alpha in mouse epididymis tissue sections by Immunohistochemistry (IHC-P - paraformaldehyde-fixed, paraffin-embedded sections). Tissue was fixed with Bouin's solution and blocked with 1.5% serum for 30 minutes at 25°C; antigen retrieval was by heat mediation in a citrate buffer. Samples were incubated with primary antibody (1/1000 in blocking buffer) for 14 hours at 4°C. Goat Anti-Rabbit IgG H&L (HRP) ab6721 Goat anti-rabbit HRP (1/200) was used as the secondary antibody.
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Glucocorticoid Receptor alpha antibody (ab3580)
ab3580 (1μg/ml) staining glucocorticoid receptor alpha in human hippocampus using an automated system (DAKO Autostainer Plus). Using this protocol there is cytoplasmic staining in the neuropil and blood vessel smooth muscle.
Sections were rehydrated and antigen retrieved with the Dako 3 in 1 AR buffer EDTA pH 9.0 in a DAKO PT Link. Slides were peroxidase blocked in 3% H2O2 in methanol for 10 mins. They were then blocked with Dako Protein block for 10 minutes (containing casein 0.25% in PBS) then incubated with primary antibody for 20 min and detected with Dako Envision Flex amplification kit for 30 minutes. Colorimetric detection was completed with Diaminobenzidine for 5 minutes. Slides were counterstained with Haematoxylin and coverslipped under DePeX. Please note that, for manual staining, optimization of primary antibody concentration and incubation time is recommended. Signal amplification may be required.