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Mouse Anti-ARSA Recombinant Antibody (CBYC-A799) (CBMAB-A3679-YC)

Provided herein is a Mouse monoclonal antibody against Human Arylsulfatase A. The antibody can be used for immunoassay techniques, such as WB, IP.
See all ARSA antibodies
Published Data
Mouse Anti-ARSA Recombinant Antibody (CBYC-A799) CBMAB-A3679-YC in WB
Representative image of ARSA (62 kDa) and β-tubulin (50 kDa) levels in ejaculated human spermatozoa, from normozoospermic men (n = 15), before and after rapid and slow freezing. ...View More
Corda, P. O., Silva, J. V., Pereira, S. C., Barros, A., Alves, M. G., & Fardilha, M. (2022). Bioinformatic approach to unveil key differentially expressed proteins in human sperm after slow and rapid cryopreservation. Frontiers in Cell and Developmental Biology, 9, 759354.

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBYC-A799
Antibody Isotype
IgG1, κ
Application
WB, IP, IF, ELISA

Basic Information

Immunogen
Amino acids 145-273 mapping within an internal region of ASA of human origin.
Specificity
Human
Antibody Isotype
IgG1, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
WB1:100-1:1,000
IP1-2 µg per 100-500 µg of total protein (1 ml of cell lysate)
IF(ICC)1:50-1:500
ELISA1:100-1:1,000

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, 0.1% gelatin
Preservative
< 0.1% sodium azide
Concentration
0.2 mg/ml
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Arylsulfatase A
Introduction
ARSA hydrolyzes cerebroside sulfate to cerebroside and sulfate. Defects in this gene lead to metachromatic leucodystrophy (MLD), a progressive demyelination disease which results in a variety of neurological symptoms and ultimately death.
Entrez Gene ID
410
UniProt ID
P15289
Alternative Names
Arylsulfatase A; Cerebroside-Sulfatase; ASA; Metachromatic Leucodystrophy; EC 3.1.6.8; EC 3.1.6; MLD;
Function
Hydrolyzes cerebroside sulfate.
Biological Process
Glycosphingolipid metabolic process Source: Reactome
Neutrophil degranulation Source: Reactome
Cellular Location
Lysosome; Endoplasmic reticulum
Involvement in disease
Metachromatic leukodystrophy (MLD): An autosomal recessive disease caused by abnormal intralysosomal accumulation of cerebroside-3-sulfate in central and peripheral nervous systems, as well as other organs. MLD is clinically characterized by leukodystrophy, progressive demyelination and a variety of neurological symptoms, including gait disturbances, ataxias, optical atrophy, dementia, seizures, and spastic tetraparesis. Decreased arylsulfatase A activity is detected in urine, leukocytes, and fibroblasts of affected individuals. Several forms of the disease can be distinguished according to the age at onset and disease severity: late infantile, juvenile and adult forms, partial cerebroside sulfate deficiency, and pseudoarylsulfatase A deficiency. Individuals with pseudoarylsulfatase A deficiency have low arylsulfatase A activity but lack neurological manifestations and are apparently healthy.
Multiple sulfatase deficiency (MSD): The protein represented in this entry is involved in disease pathogenesis. Arylsulfatase A activity is impaired in multiple sulfatase deficiency due to mutations in SUMF1 (PubMed:15146462). SUMF1 mutations result in defective post-translational modification of ARSA at residue Cys-69 that is not converted to 3-oxoalanine (PubMed:7628016). A clinically and biochemically heterogeneous disorder caused by the simultaneous impairment of all sulfatases, due to defective post-translational modification and activation. It combines features of individual sulfatase deficiencies such as metachromatic leukodystrophy, mucopolysaccharidosis, chondrodysplasia punctata, hydrocephalus, ichthyosis, neurologic deterioration and developmental delay.
PTM
The conversion to 3-oxoalanine (also known as C-formylglycine, FGly), of a serine or cysteine residue in prokaryotes and of a cysteine residue in eukaryotes, is critical for catalytic activity. This post-translational modification is severely defective in multiple sulfatase deficiency (MSD).

Xu, L., Zhong, M., Wang, Y., Wang, Z., Song, J., Zhao, J., ... & Zheng, X. (2021). Case Report: Novel Arylsulfatase A (ARSA) Gene Mutations in a Patient With Adult-Onset Metachromatic Leukodystrophy Misdiagnosed as Multiple Sclerosis. Frontiers in Neurology, 11, 1633.

Gómez-Torres, M. J., Huerta-Retamal, N., Robles-Gómez, L., Sáez-Espinosa, P., Aizpurua, J., Avilés, M., & Romero, A. (2021). Arylsulfatase A Remodeling during Human Sperm In Vitro Capacitation Using Field Emission Scanning Electron Microscopy (FE-SEM). Cells, 10(2), 222.

Yoo, H. S., Lee, J. S., Chung, S. J., Ye, B. S., Sohn, Y. H., Lee, S. J., & Lee, P. H. (2020). Changes in plasma arylsulfatase A level as a compensatory biomarker of early Parkinson’s disease. Scientific reports, 10(1), 1-6.

Ruan, Y., Zheng, R., Lin, Z. H., Gao, T., Xue, N. J., Cao, J., ... & Pu, J. L. (2020). Genetic analysis of arylsulfatase A (ARSA) in Chinese patients with Parkinson’s disease. Neuroscience Letters, 734, 135094.

Xu, L., Zhong, M., Wang, Y., Wang, Z., Song, J., Zhao, J., ... & Zheng, X. (2020). Case Report: Novel Arylsulfatase A (ARSA) Gene Mutations in a Patient With Adult-Onset Metachromatic Leukodystrophy Misdiagnosed as Multiple Sclerosis. Frontiers in Neurology, 11.

Hettiarachchi, D., & Dissanayake, V. H. W. (2020). Correction to: Three novel variants in the arylsulfatase A (ARSA) gene in patients with metachromatic leukodystrophy (MLD). BMC research notes, 13(1), 1-2.

Hettiarachchi, D., & Dissanayake, V. H. W. (2019). Three novel variants in the arylsulfatase A (ARSA) gene in patients with metachromatic leukodystrophy (MLD). BMC research notes, 12(1), 1-4.

Narayanan, D. L., Matta, D., Gupta, N., Kabra, M., Ranganath, P., Aggarwal, S., ... & Dalal, A. (2019). Spectrum of ARSA variations in Asian Indian patients with Arylsulfatase A deficient metachromatic leukodystrophy. Journal of human genetics, 64(4), 323-331.

Lee, J. S., Kanai, K., Suzuki, M., Kim, W. S., Yoo, H. S., Fu, Y., ... & Lee, S. J. (2019). Arylsulfatase A, a genetic modifier of Parkinson’s disease, is an α-synuclein chaperone. Brain, 142(9), 2845-2859.

Böhringer, J., Santer, R., Schumacher, N., Gieseke, F., Cornils, K., Pechan, M., ... & Müller, I. (2017). Enzymatic characterization of novel arylsulfatase a variants using human arylsulfatase A‐deficient immortalized mesenchymal stromal cells. Human mutation, 38(11), 1511-1520.

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For research use only. Not intended for any clinical use.

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