SAB4200166
Anti-ALS2CL (N-terminal region) 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
antigen ~125 kDa
species reactivity
human
packaging
antibody small pack of 25 μL
concentration
~1.5 mg/mL
technique(s)
western blot: 1.5-3.0 μg/mL using SH-SY5Y cell lysates.
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... ALS2CL(259173)
General description
The amyotrophic lateral sclerosis 2 (ALS2) C-terminal like (ALS2CL) gene is an ALS2 homologous gene, mapped to human chromosome 3p21.31. The encoded protein is homo-dimeric and forms an heteromeric complex with ALS2 oligomer which localize to the membrane compartments.
Specificity
Anti-ALS2CL (N-terminal region) specifically recognizes human ALS2CL.
Application
Anti-ALS2CL (N-terminal) antibody produced in rabbit is suitable for immunoblotting.
Biochem/physiol Actions
The co-expression of amyotrophic lateral sclerosis 2 (ALS2) C-terminal like (ALS2CL) along with Ras-related protein Rab-5A (Rab5) results in the distinctive tubulation phenotype of endosome compartments. It is responsible for the co-localization of ALS2CL and Rab5. ALS2CL protein has weak Rab5-guanine nucleotide exchange factor (GEF) activity, but predominantly adheres to Rab5. Also, it inhibits the ALS2 mediated endosome enlargement. ALS2CL might be considered as a critical moiety over ALS2, in modulating the ALS2 and Rab5 mediated endosome dynamics in the cell. The N-terminal region of the ALS2CL protein specifically controls endolysosomal trafficking induced by endosome-autophagosome. It is involved in the regulation of neurite growth.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
Storage and Stability
Store at −20 °C. 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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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.
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
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
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