Overview |
bs-11759R-Cy5 |
SPG3A/Atlastin Polyclonal Antibody, Cy5 Conjugated |
WB, IF(IHC-P), IF(IHC-F), IF(ICC) |
Mouse, Rat |
Human, Rabbit |
Specifications |
Cy5 |
Rabbit |
KLH conjugated synthetic peptide derived from human SPG3A/Atlastin |
201-300/558 |
Polyclonal |
IgG |
1ug/ul |
Purified by Protein A. |
Aqueous buffered solution containing 0.01M TBS (pH 7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
Store at -20°C. Aliquot into multiple vials to avoid repeated freeze-thaw cycles. |
Target |
Cytoplasm, Cell membrane |
AD FSP; atl1; ATLA1_HUMAN; Atlastin GTPase 1; Atlastin-1; Atlastin1; Brain specic GTP binding protein; Brain-specic GTP-binding protein; FSP1; GBP-3; GBP3; GTP-binding protein 3; Guanine nucleotide-binding protein 3; Guanylate binding protein 3; hGBP3; HSN1D; Spastic paraplegia 3 protein A; SPG 3A; SPG3; SPG3A. |
Atlastins are Golgi-localized, integral membrane proteins that function as GTPases. The Atlastin proteins, also designated SPG3A and guanylate-binding protein 3, comprise a Dynamin superfamily that plays a role in axonal maintenance. Hereditary spastic paraplegia (HSP) is an inherited neurodegenerative disorder that is characterized by retrograde axonal degeneration. HSP primarily affects long corticospinal neurons and causes spastic lower extremity weakness. Spastin, a microtubule (MT)-severing AAA ATPase, is a binding partner of Atlastin that is involved in membrane dynamics. This Spastin/Atlastin binding may be involved in the biochemical pathway that leads to HSP development. Mutations in the Atlastin gene (SPG3A) account for approximately 10% of all autosomal dominant HSPs, while mutations in the Spastin gene (SPG4) account for almost 40%. |
Application Dilution |
WB |
1:300-5000 |
IF(IHC-P) |
1:50-200 |
IF(IHC-F) |
1:50-200 |
IF(ICC) |
1:50-200 |