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SAB4200165

Sigma-Aldrich

Anti-ALS2CL (N-terminal) antibody produced in rabbit

~1.5 mg/mL, affinity isolated antibody

Synonym(s):

Anti-ALS2 C-terminal like

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

~125 kDa

species reactivity

human

packaging

antibody small pack of 25 μL

concentration

~1.5 mg/mL

technique(s)

indirect immunofluorescence: 1-2 μg/mL using A431 cells
western blot: 1.5-3.0 μg/mL using HepG2 cell lysates

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... ALS2CL(259173)
mouse ... Als2cl(235633)

General description

The amyotrophic lateral sclerosis 2 (ALS2) C-terminal like (ALS2CL) gene is an ALS2 homologous gene, located on human chromosome 3p21.31. It encodes a homo-dimeric protein that forms an ALS2-ALS2CL heteromeric complex with ALS2 oligomer. This complex co-localizes in the membrane compartments.

Specificity

Anti-ALS2CL (N-terminal) specifically recognizes human ALS2CL.

Application

Anti-ALS2CL (N-terminal) antibody produced in rabbit is suitable for immunoblotting.

Biochem/physiol Actions

The expression of amyotrophic lateral sclerosis 2 (ALS2) C-terminal like (ALS2CL) along with Ras-related protein Rab-5A (Rab5) causes the distinctive tubulation phenotype of endosome compartments. It also results in the co-localization of ALS2CL and Rab5. This protein possesses a weak Rab5-guanine nucleotide exchange factor (GEF) activity, but strongly binds to Rab5. Also, the ALS2CL protein suppresses the endosome enlargement induced by ALS2. In contrast to ALS2, ALS2CL might be considered as a critical moiety in modulating the ALS2 and Rab5 mediated endosome dynamics in the cell. The N-terminal region of the ALS2CL protein specifically regulates the endosome-autophagosome mediated endolysosomal trafficking. It controls the growth of neurites.

Physical form

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

Storage and Stability

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.

Disclaimer

Unless otherwise stated in our catalog, 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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Storage Class

10 - Combustible liquids

flash_point_f

Not applicable

flash_point_c

Not applicable


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Kyoko Suzuki-Utsunomiya et al.
Biochemical and biophysical research communications, 354(2), 491-497 (2007-01-24)
ALS2, the causative gene product for a number of recessive motor neuron diseases, is a guanine-nucleotide exchange factor for Rab5, and acts as a modulator for endosome dynamics. Recently, we have identified a novel ALS2 homolog, ALS2CL, which is highly
Anatoly Uzdensky et al.
Molecular neurobiology, 54(6), 4172-4188 (2016-06-22)
After ischemic stroke, cell damage propagates from infarct core to surrounding tissues (penumbra). To reveal proteins involved in neurodegeneration and neuroprotection in penumbra, we studied protein expression changes in 2-mm ring around the core of photothrombotic infarct induced in the
Ming He et al.
Arteriosclerosis, thrombosis, and vascular biology, 39(5), 902-914 (2019-03-29)
Objective- The topographical distribution of atherosclerosis in vasculature underscores the importance of shear stress in regulating endothelium. With a systems approach integrating sequencing data, the current study aims to explore the link between shear stress-regulated master transcription factor and its
Shinji Hadano et al.
FEBS letters, 575(1-3), 64-70 (2004-09-25)
ALS2, the causative gene product for juvenile recessive amyotrophic lateral sclerosis (ALS2), is a guanine-nucleotide exchange factor for the small GTPase Rab5. Here, we report a novel ALS2 homologous gene, ALS2 C-terminal like (ALS2CL), which encodes a 108-kD ALS2CL protein.

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