Mouse Anti-ARSB Recombinant Antibody (CBYC-A800) (CBMAB-A3681-YC)

Name: Mouse Anti-ARSB Recombinant Antibody (CBYC-A800)
SKU: CBMAB-A3681-YC
Rating: 5 (1 reviews)

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Published Data

Mouse Anti-ARSB Recombinant Antibody (CBYC-A800) CBMAB-A3681-YC in IF

Localization of legumain and cathepsin B in myotubes treated with or without simvastatin. Myotubes were cultured, differentiated, and incubated for 48 h without (control) or with 30 µM simvastatin prior to fixation at day 7. After fixation, the cells were permeabilized, blocked and further incubated with primary antibodies against legumain (green; A and B) or cathepsin B (green; C and D) and arylsulfatase B (ARSB; red). Secondary antibodies against the species of the primary antibodies and DAPI (blue) were used. The cells were photographed with identical camera and laser settings by LSM710 confocal microscopy (scale bars, 20 µm). ...View More

Smith, R., Solberg, R., Jacobsen, L. L., Voreland, A. L., Rustan, A. C., Thoresen, G. H., & Johansen, H. T. (2014). Simvastatin inhibits glucose metabolism and legumain activity in human myotubes. PLoS One, 9(1), e85721.

Mouse Anti-ARSB Recombinant Antibody (CBYC-A800) CBMAB-A3681-YC in Immunoblot

Subcellular localization of legumain is changed when glycosylation is inhibited. HCT116 cells were treated with DMSO (control) or 5 mg/ml tunicamycin for 24 h before lysis, isolation and enrichment of proteins in cellular fractions, electrophoresis and immunoblotting. Each lane was loaded with 7 mg total protein from the individual fractions (upper, left panel) or 30 mg total protein from total cell lysates (upper, right panel). The blots were stained with a specific legumain antibody (upper panels). Purity controls of subcellular fractions were assessed by ARSB (arylsulfatase B; soluble lysosomal protein), EEA1 (early endosomes antigen 1) and SP1 (nuclear transcription factor). One representative blot is shown (n ¼ 2). ...View More

Lunde, N. N., Haugen, M. H., Larsen, K. B. B., Damgaard, I., Pettersen, S. J., Kasem, R., ... & Solberg, R. (2017). Glycosylation is important for legumain localization and processing to active forms but not for cystatin E/M inhibitory functions. Biochimie, 139, 27-37.

Datasheet

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Basic Information

Host Animal

Mouse

Clone

CBYC-A800

Application

ICC, IF, WB

Immunogen

CHO-derived recombinant human Arylsulfatase B/ARSB, Ser37-Met533

Specificity

Human

Antibody Isotype

IgG1

Clonality

Monoclonal

Application Notes

The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Application	Note
WB	1 µg/ml
IF(ICC)	25 µg/ml

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

Format

Lyophilized

Buffer

PBS, Trehalose

Preservative

0.05 mg sodium azide

Storage

Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

More Infomation

Target

Full Name

arylsulfatase B

Introduction

Arylsulfatase B encoded by this gene belongs to the sulfatase family. The arylsulfatase B homodimer hydrolyzes sulfate groups of N-Acetyl-D-galactosamine, chondriotin sulfate, and dermatan sulfate. The protein is targeted to the lysozyme. Mucopolysacchari

Entrez Gene ID

411

UniProt ID

P15848

Alternative Names

Arylsulfatase B; N-Acetylgalactosamine-4-Sulfatase; EC 3.1.6.12; ASB; G4S; MPS6;

Function

Removes sulfate groups from chondroitin-4-sulfate (C4S) and regulates its degradation (PubMed:19306108).
Involved in the regulation of cell adhesion, cell migration and invasion in colonic epithelium (PubMed:19306108).
In the central nervous system, is a regulator of neurite outgrowth and neuronal plasticity, acting through the control of sulfate glycosaminoglycans and neurocan levels (By similarity).

Biological Process

Autophagy Source: Ensembl
Central nervous system development Source: Ensembl
Chondroitin sulfate catabolic process Source: Reactome
Colon epithelial cell migration Source: UniProtKB
Lysosomal transport Source: ProtInc
Lysosome organization Source: ProtInc
Neutrophil degranulation Source: Reactome
Positive regulation of neuron projection development Source: UniProtKB
Regulation of epithelial cell migration Source: UniProtKB
Response to estrogen Source: Ensembl
Response to methylmercury Source: Ensembl
Response to nutrient Source: Ensembl
Response to pH Source: Ensembl

Cellular Location

Lysosome; Cell surface

Involvement in disease

Mucopolysaccharidosis 6 (MPS6): An autosomal recessive lysosomal storage disease characterized by intracellular accumulation of dermatan sulfate. Clinical features can include abnormal growth, short stature, stiff joints, skeletal malformations, corneal clouding, hepatosplenomegaly, and cardiac abnormalities. A wide variation in clinical severity is observed.
Multiple sulfatase deficiency (MSD): The protein represented in this entry is involved in disease pathogenesis. Arylsulfatase B activity is impaired in multiple sulfatase deficiency due to mutations in SUMF1. SUMF1 mutations result in defective post-translational modification of ARSB at residue Cys-91 that is not converted to 3-oxoalanine. 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).

Bhattacharyya, S., Feferman, L., Han, X., Xia, K., Zhang, F., Linhardt, R. J., & Tobacman, J. K. (2020). Increased CHST15 follows decline in arylsulfatase B (ARSB) and disinhibition of non-canonical WNT signaling: potential impact on epithelial and mesenchymal identity. Oncotarget, 11(24), 2327.

Hendrickx, G., Danyukova, T., Baranowsky, A., Rolvien, T., Angermann, A., Schweizer, M., ... & Schinke, T. (2020). Enzyme replacement therapy in mice lacking arylsulfatase B targets bone-remodeling cells, but not chondrocytes. Human molecular genetics, 29(5), 803-816.

Tobacman, J. K., Bhattacharyya, S., & Feferman, L. (2020). Increased CHST15 expression follows declines in Arylsulfatase B (ARSB) and DKK3 and disinhibition of non-canonical WNT signaling.

Aminzadeh, M., Malekpour, N., & Ghandil, P. (2019). Identification of arylsulfatase B gene mutations and clinical presentations of Iranian patients with Mucopolysaccharidosis VI. Gene, 706, 1-5.

Bhattacharyya, S., Feferman, L., & Tobacman, J. K. (2019). Dihydrotestosterone inhibits arylsulfatase B and Dickkopf Wnt signaling pathway inhibitor (DKK)‐3 leading to enhanced Wnt signaling in prostate epithelium in response to stromal Wnt3A. The Prostate, 79(7), 689-700.

Pohl, S., Angermann, A., Jeschke, A., Hendrickx, G., Yorgan, T. A., Makrypidi‐Fraune, G., ... & Schinke, T. (2018). The lysosomal protein arylsulfatase B is a key enzyme involved in skeletal turnover. Journal of Bone and Mineral Research, 33(12), 2186-2201.

Bhattacharyya, S., Feferman, L., Han, X., Ouyang, Y., Zhang, F., Linhardt, R. J., & Tobacman, J. K. (2018). Decline in arylsulfatase B expression increases EGFR expression by inhibiting the protein-tyrosine phosphatase SHP2 and activating JNK in prostate cells. Journal of Biological Chemistry, 293(28), 11076-11087.

Essawi, M. L., Elbagoury, N. M., Sayed, O. M., Aglan, M. S., Ibrahim, M. M., Soliman, H. N., & Fateen, E. M. (2018). Mutation analysis of the arylsulfatase B gene among Egyptian patients with Maroteaux–Lamy disorder. Middle East Journal of Medical Genetics, 7(2), 96.

Zhang, J., Liang, H., Zhu, L., Gan, W., Tang, C., Li, J., & Xu, R. (2018). Expression and distribution of Arylsulfatase B are closely associated with neuron death in SOD1 G93A transgenic mice. Molecular neurobiology, 55(2), 1323-1337.

Bhattacharyya, S., Feferman, L., Terai, K., Dudek, A. Z., & Tobacman, J. K. (2017). Decline in arylsulfatase B leads to increased invasiveness of melanoma cells. Oncotarget, 8(3), 4169.

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Please try the standard protocols which include: protocols, troubleshooting and guide.

Enzyme-linked Immunosorbent Assay (ELISA)
Flow Cytometry
Immunofluorescence (IF)
Immunohistochemistry (IHC)
Immunoprecipitation (IP)
Western Blot (WB)
Enzyme-Linked Immunospot (ELISpot)
Proteogenomics
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