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Key Documents

SAB4200137

Sigma-Aldrich

Anti-ALS2 (N-terminal region) antibody produced in rabbit

~1.5 mg/mL, affinity isolated antibody

Sinonimo/i:

Anti-ALS2CR6, Anti-ALSIN, Anti-ALSJ, Anti-IAHSP, Anti-PLSJ

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About This Item

Codice UNSPSC:
12352203
NACRES:
NA.41

Origine biologica

rabbit

Coniugato

unconjugated

Forma dell’anticorpo

affinity isolated antibody

Tipo di anticorpo

primary antibodies

Clone

polyclonal

Forma fisica

buffered aqueous solution

PM

antigen ~185 kDa

Confezionamento

antibody small pack of 25 μL

Concentrazione

~1.5 mg/mL

tecniche

indirect immunofluorescence: 2-4 μg/mL using NIH3T3 cells
western blot: 1.5-3.0 μg/mL using HEK-293T cell lysate over expressing human ALS2, and rat cerebellum extract (S1 fraction).

Condizioni di spedizione

dry ice

Temperatura di conservazione

−20°C

modifica post-traduzionali bersaglio

unmodified

Informazioni sul gene

mouse ... Als2(74018)
rat ... Als2(363235)

Descrizione generale

Amyotrophic lateral sclerosis (ALS)2 gene codes for 184 kDa alsin protein. Alsin is characterized with the three putative guanine exchange factor (GEF) domains such as, RCC1-like domain (RLD), the Dbl and pleckstrin homology (DH/PH) domain, and a vacuolar protein sorting 9 (VPS9) domain. In addition, ALS2 also contains eight consecutive membrane occupation and recognition nexus (MORN) motifs. ALS2 mRNA is ubiquitously expressed in the CNS and non-neuronal tissues, with the highest expression in the cerebellum and kidney.

Specificità

Anti-ALS2 (N-terminal region) specifically recognizes human, rat, and mouse ALS2.

Applicazioni

Anti-ALS2 (N-terminal region) antibody produced in rabbit has been used in immunoblotting and immunoprecipitation.

Azioni biochim/fisiol

Amyotrophic lateral sclerosis (ALS)2 has been shown to mediate the activation of Rab5 and Rac1/PACK1. In the nervous system, ALS2 is preferentially associated with the cytoplasmic side of endosome membrane, it modulates endosome membrane trafficking and promotes neurite growth in neuronal cultures. Loss-of function mutations in the ALS2 gene leads to the development of recessive motor neuron diseases, including forms of ALS (ALS2), juvenile PLS (PLSJ) and hereditary spastic paraplegia (HSP).

Stato fisico

Solution in 0.01 M phos­phate buffered saline, pH 7.4, containing 15 mM sodium azide.

Stoccaggio e stabilità

For continuous use, store at 2–8 °C for up to one month. For extended storage, freeze in working aliquots. Repeated freezing and thawing, or storage in “frost-free” freezers, is not recommended. If slight turbidity occurs upon prolonged storage, clarify the solution by centrifugation before use. Working dilutions should be discarded if not used within 12 hours.

Esclusione di responsabilità

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Codice della classe di stoccaggio

10 - Combustible liquids

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable


Certificati d'analisi (COA)

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I documenti relativi ai prodotti acquistati recentemente sono disponibili nell’Archivio dei documenti.

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Alsin and the Molecular Pathways of Amyotrophic Lateral Sclerosis
Chandran J, et al.
Molecular Neurobiology, 36, 224-224 (2007)
Mice deficient in the Rab5 guanine nucleotide exchange factor ALS2/alsin exhibit age-dependent neurological deficits and altered endosome trafficking
Hadano S, et al.
Human Molecular Genetics, 15, 233-250 (2005)
Gönenç Çobanoğlu et al.
Biochemical and biophysical research communications, 427(1), 1-4 (2012-09-18)
Mutations in ALS2 gene/alsin are associated with recessive forms of motor neuron disorders including Juvenile Amyotrophic Lateral Sclerosis (JALS), Infantile-onset Ascending Hereditary Spastic Paraplegia (IAHSP) and Juvenile Primary Lateral Sclerosis (JPLS). In this study, we show that alsin and another
The Rab5 Activator ALS2/alsin Acts as a Novel Rac1 Effector through Rac1-activated Endocytosis
Kunita R, et al.
The Journal of Biological Chemistry, 282, 16599-16611 (2007)
Izzet Enunlu et al.
Biochemical and biophysical research communications, 413(3), 471-475 (2011-09-13)
Mutations in Als2 gene cause several autosomal recessive forms of motor neuron diseases including Juvenile Amyotrophic Lateral Sclerosis (JALS), Juvenile Primary Lateral Sclerosis (PLSJ) and Infantile-onset Ascending Hereditary Spastic Paralysis (IAHSP). To find novel protein-protein interactions of Als2 protein we

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