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CSF2RA Human

GM-CSF Receptor Alpha Human Recombinant

 
Catalog #
GRF0015
Uniprot Id
P15509
 
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 Catalog #AvailabilitySizeQuantityUnit Price Save For Later Wish List
GRF0015-5 7 days 5 µg $120.00
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GRF0015-20 7 days 20 µg $290.00
GRF0015-1 7 days 1 mg $4,320.00
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Product Overview

NameCSF2RA Human
Description
GM-CSF Receptor Alpha Human Recombinant
Accession (Primary)P15509
Synonyms
Colony Stimulating Factor 2 Receptor Alpha Subunit, Colony Stimulating Factor 2 Receptor, Alpha, Low-Affinity (Granulocyte-Macrophage), Alpha-GM-CSF Receptor, GM-CSF-R-Alpha, CD116 Antigen, GMCSFR-Alpha, GMR-Alpha, CDw116, CSF2RY, CSF2R, Granulocyte-Macrophage Colony-Stimulating Factor Receptor Subunit Alpha, Granulocyte-Macrophage Colony-Stimulating Factor Receptor Alpha Chain, GM-CSF Receptor Alpha Subunit, AlphaGMR, CSF2RAX, CSF2RAY, CSF2RX, GMCSFR, CD116, SMDP4, GMR.
Introduction
GM-CSF Receptor Alpha (CSF2RA) is the alpha subunit of the heterodimeric receptor for colony stimulating factor 2, a cytokine which controls the production, differentiation, and function of granulocytes and macrophages. CSFR2 is also a member of the cytokine family of receptors. In addition, this gene is found in the pseudoautosomal region (PAR) of the X and Y chromosomes. Multiple transcript variants encoding various isoforms have been found for this gene, while some of the isoforms being membrane-bound and others being soluble. Diseases associated with CSF2RA include surfactant metabolism dysfunction, pulmonary 4, and csf2ra-related pulmonary surfactant metabolism dysfunction.
Source
Sf9, Baculovirus cells.
Physical Appearance
Sterile Filtered colorless solution.
Formulation
CSF2RA protein solution (0.5mg/ml) contains Phosphate Buffered Saline (pH 7.4) and 10% glycerol.
Stability
Store at 4°C if entire vial will be used within 2-4 weeks. Store, frozen at -20°C for longer periods of time. For long term storage it is recommended to add a carrier protein (0.1% HSA or BSA). Avoid multiple freeze-thaw cycles.
Purity
Greater than 90.0% as determined by SDS-PAGE.
Amino acid sequence
ADP LIPEKSD LRTVAPASSL NVRFDSRTMN LSWDCQENTT FSKCFLTDKK NRVVEPRLSN NECSCTFREI CLHEGVTFEV HVNTSQRGFQ QKLLYPNSGR EGTAAQNFSC FIYNADLMNC TWARGPTAPR DVQYFLYIRN SKRRREIRCP YYIQDSGTHV GCHLDNLSGL TSRNYFLVNG TSREIGIQFF DSLLDTKKIE RFNPPSNVTV RCNTTHCLVR WKQPRTYQKL SYLDFQYQLD VHRKNTQPGT ENLLINVSGD LENRYNFPSS EPRAKHSVKI RAADVRILNW SSWSEAIEFG SDDG HHHHHH
Biological Activity
Measured by its ability to inhibit GM-CSF dependent proliferation of TF1 human erythroleukemic cells. The ED50 for this effect is less or equal to 10ug/ml in the presence of 0.5ng/ml GM-CSF.
Background
GM-CSF Receptor Alpha Human Recombinant: A Glimpse into Its Potential and Implications Abstract: Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) receptor alpha, a pivotal component in the GM-CSF signaling pathway, has been the focal point of numerous studies pertaining to hematopoiesis and immune responses. This paper provides an overview of the GM-CSF receptor alpha human recombinant, exploring its characteristics, production techniques, and potential therapeutic applications. Introduction GM-CSF, a cytokine responsible for the differentiation and proliferation of white blood cells, functions by binding to its receptor, GM-CSF receptor. The alpha subunit (GM-CSFRα) of this receptor plays a crucial role in ligand binding and is essential for initiating cellular responses. Modern biotechnological advancements have led to the successful production of its human recombinant form, offering new avenues in medical research. Recombinant GM-CSFRα: Production and Features Recombinant GM-CSFRα is synthesized using cutting-edge recombinant DNA technologies, predominantly in bacterial or mammalian expression systems. This human recombinant form retains its ability to bind to GM-CSF, maintaining its biological functionality and providing myriad research opportunities. Therapeutic and Clinical Prospects Autoimmune Diseases: GM-CSF is often overexpressed in various autoimmune disorders. By utilizing recombinant GM-CSFRα as a potential decoy receptor, it's feasible to mitigate the effects of excessive GM-CSF, offering a new therapeutic strategy. Hematopoietic Disorders: Given its integral role in white blood cell development, recombinant GM-CSFRα might hold promise in treatments or as a diagnostic tool for certain hematological conditions. Research Paradigm: Beyond therapeutic applications, the recombinant GM-CSFRα can serve as an invaluable research tool to elucidate the nuances of GM-CSF signaling, aiding in the understanding of immune response mechanisms. Conclusion: GM-CSF receptor alpha human recombinant stands at the forefront of exciting research and therapeutic potential. While its full capabilities are yet to be realized, current insights underscore its significance in the realms of immunology and medicine.
References
Bibliography Burgess, A. W., & Metcalf, D. (1980). The nature and action of granulocyte-macrophage colony-stimulating factors. Blood , 56(6), 947-958. Hamilton, J. A. (2008). GM-CSF in inflammation and autoimmunity. Trends in Immunology , 23(8), 403-408. Hercus, T. R., et al. (2009). The granulocyte-macrophage colony-stimulating factor receptor: Linking its structure to cell signaling. Blood , 114(7), 1289-1298. Lehtonen, A., Matikainen, S., & Julkunen, I. (2002). Interferons up-regulate STAT1, STAT2, and IRF family transcription factor gene expression in human peripheral blood mononuclear cells and macrophages. Journal of Immunology , 169(1), 358-368.
Precautions
CSF2RA Human is for research use only and not for use in diagnostic or therapeutic procedures.

Target Information: ( P15509 )

Background

Unlocking the Potential of Human Recombinant Ciliary Neurotrophic Factor Receptor: Implications and Applications Abstract: The Ciliary Neurotrophic Factor Receptor (CNTFR) plays a pivotal role in mediating the effects of ciliary neurotrophic factor (CNTF) on neuronal survival and growth. This paper examines the significance of Human Recombinant CNTFR, its production techniques, and its potential applications in neurobiology and therapeutic interventions. The review underscores CNTFR's crucial role in advancing neuroprotection and neuroregeneration research. Introduction: CNTFR, a transmembrane protein, is central to transducing the signals initiated by CNTF. Availability of Human Recombinant CNTFR enables researchers to dissect its contribution to neuronal function and develop targeted therapies for neurodegenerative disorders. CNTFR's role in modulating neuronal health and promoting regeneration makes it a cornerstone in neurobiology. Role in CNTF Signaling: CNTFR forms a receptor complex with other proteins, including gp130 and LIFRβ, to bind CNTF and trigger downstream signaling pathways. Activation of intracellular cascades, such as JAK/STAT and MAPK, is instrumental in driving the neuroprotective and growth-promoting effects of CNTF. Production Methods: Human Recombinant CNTFR is generated through gene expression in suitable host cells, often utilizing bacterial or mammalian systems. Ensuring accurate folding and post-translational modifications is crucial to preserve its functionality and affinity for CNTF. Therapeutic Applications: Human Recombinant CNTFR holds promise for therapeutic applications in neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), multiple sclerosis, and retinal degeneration. Manipulating CNTFR-associated signaling presents opportunities to bolster neuronal survival and regeneration, potentially revolutionizing patient care. Challenges and Future Directions: While the potential is significant, challenges encompass optimizing CNTFR-CNTF interactions, effective tissue delivery, and understanding potential off-target effects. Ongoing research is paramount to unravel the complete mechanisms of CNTFR-mediated signaling and its therapeutic implications. Conclusion: Human Recombinant Ciliary Neurotrophic Factor Receptor emerges as a vital tool in advancing our grasp of neuroprotection and regeneration. Its capacity to modulate CNTF effects opens doors to innovative therapeutic strategies for addressing neurodegenerative disorders, embodying the intersection of molecular insights and clinical progress.

References

Bibliography: Ip NY, Yancopoulos GD. The neurotrophins and CNTF: Collaborative neurotrophic factors. Annu Rev Neurosci. 1996;19:491-515. Sendtner M. The biology of neurotrophic factors. J Neurobiol. 1994;25(11):1384-1403. Davis S, Aldrich TH, Valenzuela DM, et al. The receptor for ciliary neurotrophic factor. Science. 1991;253(5015):59-63. Benveniste EN, Benveniste P, Shaffer K. Ciliary neurotrophic factor promotes the glial differentiation of rat cortical precursor cells. J Neurosci Res. 1993;36(6):607-614. DeChiara TM, Vejsada R, Poueymirou WT, et al. Mice lacking the CNTF receptor, unlike mice lacking CNTF, exhibit profound motor neuron deficits at birth. Cell. 1995;83(2):313-322.

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