Weight | 1 lbs |
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Dimensions | 9 × 5 × 2 in |
host | mouse |
isotype | IgG1 |
clonality | monoclonal |
concentration | 1 mg/mL |
applications | ICC/IF, IHC, WB |
reactivity | human, mouse, rat |
available sizes | 1 mg, 100 µg, 25 µg |
mouse anti-GFAP monoclonal antibody (5C10) 3743
$100.00 – $2,600.00
Antibody summary
- Mouse monoclonal to GFAP
- Suitable for: WB, ICC/IF, IHC
- Reacts with: human, mouse, rat
- Isotype: IgG1
- 100 µg, 25 µg, 1 mg
mouse anti-GFAP monoclonal antibody (5C10) 3743
target relevance |
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Glial Fibrillary Acidic Protein (GFAP) is a crucial cell marker widely employed in neuroscience and neurobiology research. It is an intermediate filament protein primarily found in astrocytes, a type of glial cell in the central nervous system. GFAP serves as a reliable marker for identifying and characterizing astrocytes in various experimental models and tissues. Immunohistochemistry and immunofluorescence techniques using antibodies targeting GFAP enable researchers to visualize and quantify astrocytic populations, gaining insights into their distribution, morphology, and function in the brain. Moreover, GFAP antibodies are instrumental in studying astrocyte reactivity, a phenomenon occurring in response to brain injury or neurodegenerative diseases. As astrocytes play critical roles in neural development, neurotransmitter regulation, and maintenance of the blood-brain barrier, GFAP has proven indispensable in advancing our understanding of glial biology and its contribution to neurological disorders. Click for more on: cell markers and GFAP |
Protein names Glial fibrillary acidic protein (GFAP) |
Gene names GFAP,GFAP |
Protein family Intermediate filament family |
Mass 49880Da |
Function GFAP, a class-III intermediate filament, is a cell-specific marker that, during the development of the central nervous system, distinguishes astrocytes from other glial cells. |
Subellular location Cytoplasm Note=Associated with intermediate filaments. |
Tissues Expressed in cells lacking fibronectin. |
Structure Interacts with SYNM. ; [Isoform 2]: Interacts with PSEN1 (via N-terminus). |
Post-translational modification Phosphorylated by PKN1. |
Involvement in disease Alexander disease (ALXDRD) [MIM:203450]: A rare disorder of the central nervous system. The most common form affects infants and young children, and is characterized by progressive failure of central myelination, usually leading to death within the first decade. Infants with Alexander disease develop a leukodystrophy with macrocephaly, seizures, and psychomotor retardation. Patients with juvenile or adult forms typically experience ataxia, bulbar signs and spasticity, and a more slowly progressive course. Histologically, Alexander disease is characterized by Rosenthal fibers, homogeneous eosinophilic inclusions in astrocytes. Note=The disease is caused by variants affecting the gene represented in this entry. |
Target Relevance information above includes information from UniProt accession: P14136 |
The UniProt Consortium |
Data
Publications
Publications
pmid | title | authors | citation |
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37237366 | Reactive Bergmann glia play a central role in spinocerebellar ataxia inflammation via the JNK pathway. | Chandrakanth Reddy Edamakanti, Vishwa Mohan, Puneet Opal | J Neuroinflammation 20:126 |
35839339 | Enhanced nociceptive behavior and expansion of associated primary afferents in a rabbit model of cerebral palsy. | Emily J Reedich, Landon T Genry, Meredith A Singer, Clarissa Fantin Cavarsan, Elvia Mena Avila, Daphne M Boudreau, Michael C Brennan, Alyssa M Garrett, Lisa Dowaliby, Megan R Detloff, Katharina A Quinlan | J Neurosci Res 100:1951-1966 |
35203460 | Mitoquinone Helps Combat the Neurological, Cognitive, and Molecular Consequences of Open Head Traumatic Brain Injury at Chronic Time Point. | Muhammad Ali Haidar, Zaynab Shakkour, Chloe Barsa, Maha Tabet, Sarin Mekhjian, Hala Darwish, Mona Goli, Deborah Shear, Jignesh D Pandya, Yehia Mechref, Riyad El Khoury, Kevin Wang, Firas Kobeissy | Biomedicines 10:N/A |
35065054 | Mitoquinone supplementation alleviates oxidative stress and pathologic outcomes following repetitive mild traumatic brain injury at a chronic time point. | Maha Tabet, Marya El-Kurdi, Muhammad Ali Haidar, Leila Nasrallah, Mohammad Amine Reslan, Deborah Shear, Jignesh D Pandya, Ahmed F El-Yazbi, Mirna Sabra, Stefania Mondello, Yehia Mechref, Abdullah Shaito, Kevin K Wang, Riyad El-Khoury, Firas Kobeissy | Exp Neurol 351:113987 |
33124191 | SATB2 drives glioblastoma growth by recruiting CBP to promote FOXM1 expression in glioma stem cells. | Weiwei Tao, Aili Zhang, Kui Zhai, Zhi Huang, Haidong Huang, Wenchao Zhou, Qian Huang, Xiaoguang Fang, Briana C Prager, Xiuxing Wang, Qiulian Wu, Andrew E Sloan, Manmeet S Ahluwalia, Justin D Lathia, Jennifer S Yu, Jeremy N Rich, Shideng Bao | EMBO Mol Med 12:e12291 |
Protocols
relevant to this product |
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Western blot IHC ICC |
Documents
# | SDS | Certificate | |
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