SPG11 polyclonal antibody
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Specification
Product Description
Rabbit polyclonal antibody raised against synthetic peptide of SPG11.
Immunogen
A synthetic peptide corresponding to 15 amino acids near C-terminus of human SPG11.
Host
Rabbit
Reactivity
Human, Mouse, Rat
Form
Liquid
Purification
Peptide affinity purification
Concentration
1 mg/mL
Recommend Usage
Western Blot (0.5-1 ug/mL)
Immunohistochemistry (2.5 ug/mL)
The optimal working dilution should be determined by the end user.Storage Buffer
In PBS (0.02% sodium azide)
Storage Instruction
Store at 4°C for three months. For long term storage store at -20°C.
Aliquot to avoid repeated freezing and thawing.Note
This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
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Applications
Western Blot (Tissue lysate)
Western blot analysis of SPG11 in mouse heart tissue lysate with SPG11 polyclonal antibody (Cat # PAB16698) at (A) 0.5 and (B) 1 ug/mL .Immunohistochemistry
Immunohistochemical staining of mouse brain tissue with 2.5 ug/mL SPG11 polyclonal antibody (Cat # PAB16698).Enzyme-linked Immunoabsorbent Assay
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Gene Info — SPG11
Entrez GeneID
80208Protein Accession#
AAI53880Gene Name
SPG11
Gene Alias
DKFZp762B1512, FLJ21439, KIAA1840, SPATACSIN
Gene Description
spastic paraplegia 11 (autosomal recessive)
Gene Ontology
HyperlinkGene Summary
The protein encoded by this gene is a potential transmembrane protein that is phosphorylated upon DNA damage. Defects in this gene are a cause of spastic paraplegia type 11 (SPG11). Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq
Other Designations
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Interactome
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Disease
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Publication Reference
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SPG11 mutations cause Kjellin syndrome, a hereditary spastic paraplegia with thin corpus callosum and central retinal degeneration.
Orlen H, Melberg A, Raininko R, Kumlien E, Entesarian M, Soderberg P, Pahlman M, Darin N, Kyllerman M, Holmberg E, Engler H, Eriksson U, Dahl N.
American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics 2009 Oct; 150B(7):984.
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Point mutations and a large intragenic deletion in SPG11 in complicated spastic paraplegia without thin corpus callosum.
Crimella C, Arnoldi A, Crippa F, Mostacciuolo ML, Boaretto F, Sironi M, D'Angelo MG, Manzoni S, Piccinini L, Turconi AC, Toscano A, Musumeci O, Benedetti S, Fazio R, Bresolin N, Daga A, Martinuzzi A, Bassi MT.
Journal of Medical Genetics 2009 Feb; 46(5):345.
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SPG11 mutations are common in familial cases of complicated hereditary spastic paraplegia.
Paisan-Ruiz C, Dogu O, Yilmaz A, Houlden H, Singleton A.
Neurology 2008 Apr; 70(16 Pt 2):1384.
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SPG11 mutations cause Kjellin syndrome, a hereditary spastic paraplegia with thin corpus callosum and central retinal degeneration.
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