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MABN1831

Sigma-Aldrich

Anti-Atlastin-1 Antibody, clone 3194

clone 3194, from mouse

Synonym(s):

Atlastin-1, Brain-specific GTP-binding protein, GBP-3, GTP-binding protein 3, Guanine nucleotide-binding protein 3, hGBP3, Spastic paraplegia 3 protein A

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41

biological source

mouse

Quality Level

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

3194, monoclonal

species reactivity

mouse, rat, human

species reactivity (predicted by homology)

monkey (based on 100% sequence homology)

technique(s)

immunocytochemistry: suitable
western blot: suitable

isotype

IgG2aκ

NCBI accession no.

UniProt accession no.

target post-translational modification

unmodified

Gene Information

human ... ATL1(51062)

General description

Atlastin-1 (UniProt Q8WXF7; also known as Brain-specific GTP-binding protein, GBP-3, GTP-binding protein 3, Guanine nucleotide-binding protein 3, hGBP3, Spastic paraplegia 3 protein A) is encoded by the ATL1 (also known as GBP3, HSN1D, SPG3, SPG3A) gene (Gene ID 51062) in human. Atlastin-1 is a dynamin/Mx/guanylate-binding protein superfamily member with three conserved guanylate-binding/GTPase active site motifs, P-loop (a.a. 74-81), DxxG (a.a. 146-149), and RD (217-218). Atlastin-1 is a multimeric integral membrane protein localized on ER and cis-Golgi apparatus and widely expressed in many tissues, including the smooth muscle, adrenal gland, kidney, testis, lung, and brain. Atlastin-1 interacts with the microtubule-severing ATPase spastin as well as with the DP1/Yop1p and reticulon families of ER-shaping proteins, Atlastin-1 knockdown results in decreased number of neuronal processes and impaired axon formation in cultured cortical neurons, while atlastin-1 overexpression increases total dendrite length both in vivo and in vitro. ALT1 gene mutations cause abnormal ER morphology and are linked to hereditary spastic paraplegias (HSPs), a genetically heterogeneous group of neurological disorders, includiing SPG3 (spastic paraplegia 3, autosomal dominan) and HSN1D (neuropathy, hereditary sensory, 1D), characterized by lower limb spasticity and weakness. Human atlastin-1 is a 492-amino acid protein that passes through the ER membrane twice (a.a. 450-470, 472-492), having both its N- and C-terminal ends at the cytoplasmic side (a.a. 1-449, 493-558).

Specificity

Clone 3194 targets an N-terminal epitope present in both spliced isoforms of human Atlastin-1 reported by UniProt (Q8WXF7).

Immunogen

Linear peptide corresponding to the N-terminal sequence of human Atlastin-1.

Application

Anti-Atlastin-1 Antibody, clone 3194 is an antibody against Atlastin-1 for use in Western Blotting, Immunocytochemistry.
Western Blotting Analysis: 10 µg/mL from a representative lot detected Atlastin-1 in 10 µg of mouse brain tissue lysate.
Immunocytochemistry Analysis: A representative lot localized Atlastin-1 immunoreactivity with that of REEP1 by dual fluorescent immunocytochemistry staining of paraformaldehyde-fixed rat cortical neurons (Park, S.H., et al. (2010). J. Clin. Invest. 120(4):1097-1110).
Immunocytochemistry Analysis: A representative lot localized overexpressed human Atlastin-1 in paraformaldehyde-fixed COS7 transfectants by fluorescent immunocytochemistry (Park, S.H., et al. (2010). J. Clin. Invest. 120(4):1097-1110).

Quality

Evaluated by Western Blotting in human brain tissue lysate.

Western Blotting Analysis: 2.0 µg/mL of this antibody detected Atlastin-1 in 10 µg of human brain tissue lysate.

Target description

~63 kDa observed. 63.54/63.06 (human isoform 1/2), 63.52 kDa (monkey), and 63.38 kDa (mouse and rat) calculated.

Physical form

Format: Purified

Other Notes

Concentration: Please refer to lot specific datasheet.

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Storage Class Code

12 - Non Combustible Liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

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Xiangling Meng et al.
Nature, 622(7982), 359-366 (2023-09-28)
The assembly of cortical circuits involves the generation and migration of interneurons from the ventral to the dorsal forebrain1-3, which has been challenging to study at inaccessible stages of late gestation and early postnatal human development4. Autism spectrum disorder and

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