产品名称
Anti-Glial Fibrillary Acidic Protein Rat mAb (2.2B10), liquid, clone 2.2B10, Calbiochem®
biological source
rat
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
dilution
(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))
isotype
IgG2a
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Quality Level
Gene Information
human ... GCM1(8521)
Analysis Note
Positive Control
Human or rat brain tissues
Human or rat brain tissues
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)
Disclaimer
Toxicity: Standard Handling (A)
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
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.
Packaging
Please refer to vial label for lot-specific concentration.
Physical form
In PBS.
Preparation Note
Following initial thaw, aliquot and freeze (-20°C).
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
未找到合适的产品？
试试我们的产品选型工具.
存储类别
11 - Combustible Solids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
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
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
Homocysteine fibrillar assemblies display cross-talk with Alzheimer's disease β-amyloid polypeptide.
Dorin Sade Yazdi et al.
Proceedings of the National Academy of Sciences of the United States of America, 118(24) (2021-06-09)
High levels of homocysteine are reported as a risk factor for Alzheimer's disease (AD). Correspondingly, inborn hyperhomocysteinemia is associated with an increased predisposition to the development of dementia in later stages of life. Yet, the mechanistic link between homocysteine accumulation
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
我们的科学家团队拥有各种研究领域经验，包括生命科学、材料科学、化学合成、色谱、分析及许多其他领域.
联系客户支持