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MABN1831

Sigma-Aldrich

Anti-Atlastin-1 Antibody, clone 3194

clone 3194, from mouse

Synonyme(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

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

Source biologique

mouse

Niveau de qualité

Forme d'anticorps

purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

3194, monoclonal

Espèces réactives

mouse, rat, human

Réactivité de l'espèce (prédite par homologie)

monkey (based on 100% sequence homology)

Technique(s)

immunocytochemistry: suitable
western blot: suitable

Isotype

IgG2aκ

Numéro d'accès NCBI

Numéro d'accès UniProt

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... ATL1(51062)

Description générale

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).

Spécificité

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

Immunogène

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).

Qualité

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.

Description de la cible

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

Forme physique

Format: Purified

Autres remarques

Concentration: Please refer to lot specific datasheet.

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Code de la classe de stockage

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

WGK 1

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Consulter la Bibliothèque de documents

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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