345860
Anti-Glial Fibrillary Acidic Protein Rat mAb (2.2B10)
liquid, clone 2.2B10, Calbiochem®
Synonym(s):
Anti-GFAP
Sign Into View Organizational & Contract Pricing
All Photos(1)
About This Item
UNSPSC Code:
12352203
NACRES:
NA.41
Recommended Products
biological source
rat
Quality Level
antibody form
purified antibody
antibody product type
primary antibodies
clone
2.2B10, monoclonal
form
liquid
contains
≤0.1% sodium azide as preservative
species reactivity
bovine, rat, mouse, human
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
avoid repeated freeze/thaw cycles
isotype
IgG2a
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... GCM1(8521)
General description
Purified rat monoclonal antibody. Recognizes the ~55 kDa glial fibrillary acidic protein (GFAP).
Recognizes GFAP in astrocytes induced by a variety of CNS injuries in human and rat brain tissues.
This Anti-Glial Fibrillary Acidic Protein Rat mAb (2.2B10) is validated for use in ELISA, Immunoblotting, Frozen Sections, IP, Paraffin Sections for the detection of Glial Fibrillary Acidic Protein.
Immunogen
Bovine Brain
bovine GFAP
Application
ELISA (0.1-0.5 µg/ml)
Immunoblotting (0.1-0.5 µg/ml)
Frozen Sections (10-50 µg/ml)
Immunoprecipitation (2-5 µg/ml)
Paraffin Sections (10-50 µg/ml, see comments)
Immunoblotting (0.1-0.5 µg/ml)
Frozen Sections (10-50 µg/ml)
Immunoprecipitation (2-5 µg/ml)
Paraffin Sections (10-50 µg/ml, see comments)
Packaging
Please refer to vial label for lot-specific concentration.
Warning
Toxicity: Standard Handling (A)
Physical form
In PBS.
Reconstitution
Following initial thaw, aliquot and freeze (-20°C).
Analysis Note
Positive Control
Human or rat brain tissues
Human or rat brain tissues
Other Notes
Product is not to be used for animal treatment, in vivo research, or in any other contact procedure with livestock. Stains reactive rodent and human brain astrocytes induced by a variety of central nervous system injuries. This antibody is suitable for immunohistochemical staining of Bouin′s-fixed, frozen, or paraffin-embedded tissue sections. Variables associated with assay conditions will dictate the proper working dilution.
Tohyama, T., et al. 1993. Am. J. Pathol.142, 871.
Lee, V.M., et al. 1984. J. Neurochem. 42, 25.
Lee, V.M., et al. 1984. J. Neurochem. 42, 25.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
Not finding the right product?
Try our Product Selector Tool.
Storage Class Code
11 - Combustible Solids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
Already Own This Product?
Find documentation for the products that you have recently purchased in the Document Library.
Michael S Petrik et al.
Neuromolecular medicine, 9(1), 83-100 (2006-11-23)
Gulf War illness (GWI) affects a significant percentage of veterans of the 1991 conflict, but its origin remains unknown. Associated with some cases of GWI are increased incidences of amyotrophic lateral sclerosis and other neurological disorders. Whereas many environmental factors
Flora Guillot et al.
Journal of neuroinflammation, 12, 130-130 (2015-07-05)
Astrocytes, the most abundant cell population in mammal central nervous system (CNS), contribute to a variety of functions including homeostasis, metabolism, synapse formation, and myelin maintenance. White matter (WM) reactive astrocytes are important players in amplifying autoimmune demyelination and may
Tadasuke Tominaga et al.
PloS one, 14(3), e0213673-e0213673 (2019-03-12)
Primary and secondary traumatic brain injury (TBI) can cause tissue damage by inducing cell death pathways including apoptosis, necroptosis, and autophagy. However, similar pathways can also lead to senescence. Senescent cells secrete senescence-associated secretory phenotype proteins following persistent DNA damage
Marco Foddis et al.
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 40(2), 276-287 (2019-09-25)
Brain collateral circulation is an essential compensatory mechanism in response to acute brain ischemia. To study the temporal evolution of brain macro and microcollateral recruitment and their reciprocal interactions in response to different ischemic conditions, we applied a combination of
Ulrich F O Luhmann et al.
Human molecular genetics, 24(1), 128-141 (2014-08-26)
Understanding phenotype-genotype correlations in retinal degeneration is a major challenge. Mutations in CRB1 lead to a spectrum of autosomal recessive retinal dystrophies with variable phenotypes suggesting the influence of modifying factors. To establish the contribution of the genetic background to
Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.
Contact Technical Service