Rabbit Anti-Human CTSB (a.a. 251-339) Polyclonal antibody

Name: Rabbit Anti-Human CTSB (a.a. 251-339) Polyclonal antibody
SKU: DPABH-25697
Rating: 5 (1 reviews)

Rabbit Anti-Human CTSB (a.a. 251-339) Polyclonal antibody for WB, IHC-P, IHC-F, IF, FC

COA

SDS

Datasheet

Key features and details

Target: CTSB
Host: Rabbit
Application: WB, IHC-P, IHC-F, IF, FC
Species Reactivity: Human, Mouse, Rat

Summary

Specifications

Antibody Isotype

IgG

Species Reactivity

Human; Mouse; Rat

Immunogen

KLH conjugated synthetic peptide derived from human Cathepsin B heavy chain: 251-339/339

Conjugate

Unconjugated

Applications

Application Notes

WB: 1:500-2000
IHC-P: 1:100-500
IHC-F: 1:100-500
IF: 1:100-500
Flow-Cyt: 1μg/Test

General Notes

This product (Catalog No. DPABH-25697) is a rabbit-derived IgG polyclonal antibody raised against human CTSB, targeting the amino acid region 251–339 of the protein. This antibody exhibits cross-reactivity with CTSB from mouse and rat. It has been affinity purified by Protein A. This gene encodes a member of the C1 family of peptidases. Alternative splicing of this gene results in multiple transcript variants. At least one of these variants encodes a preproprotein that is proteolytically processed to generate multiple protein products. These products include the cathepsin B light and heavy chains, which can dimerize to form the double chain form of the enzyme. This enzyme is a lysosomal cysteine protease with both endopeptidase and exopeptidase activity that may play a role in protein turnover. It is also known as amyloid precursor protein secretase and is involved in the proteolytic processing of amyloid precursor protein (APP). Incomplete proteolytic processing of APP has been suggested to be a causative factor in Alzheimer's disease, the most common cause of dementia. Overexpression of the encoded protein has been associated with esophageal adenocarcinoma and other tumors. Both Cathepsin B and Cathepsin L are involved in the cleavage of the spike protein from the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) upon its entry to the human host cell. Multiple pseudogenes of this gene have been identified.
DPABH-25697 is suitable for use in Western blot (WB) (1:500–1:2,000), IHC-P (1:100–1:500), IHC-F (1:100–1:500), IF (immunofluorescence) (1:100–1:500), flow cytometry (FC) (1 μg/test) applications.
DPABH-25697 is supplied as a liquid formulation in 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. For long-term storage, keep at −20 °C. For short-term use, store at 2–8 °C. Avoid repeated freeze–thaw cycles to maintain antibody integrity and performance.

Target

Alternative Names

Amyloid precursor protein secretase; APP secretase; APPS; Cathepsin B; CB; Cathepsin B1; CathepsinB; CPSB; CTSB; Cysteine protease; Preprocathepsin B; Cathepsin B heavy chain; Cathepsin B light chain; CATB_HUMAN

Entrez Gene ID

1508

UniProt ID

P07858

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

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References

Deletion of Cysteine Cathepsins B or L Yields Differential Impacts on Murine Skin Proteome and Degradome

MOLECULAR & CELLULAR PROTEOMICS

Authors: Tholen, Stefan; Biniossek, Martin L.; Gansz, Martina; Gomez-Auli, Alejandro; Bengsch, Fee; Noel, Agnes; Kizhakkedathu, Jayachandran N.; Boerries, Melanie; Busch, Hauke; Reinheckel, Thomas; Schilling, Oliver

Abstract

Numerous studies highlight the fact that concerted proteolysis is essential for skin morphology and function. The cysteine protease cathepsin L (Ctsl) has been implicated in epidermal proliferation and desquamation, as well as in hair cycle regulation. In stark contrast, mice deficient in cathepsin B (Ctsb) do not display an overt skin phenotype. To understand the systematic consequences of deleting Ctsb or Ctsl, we determined the protein abundances of > 1300 proteins and proteolytic cleavage events in skin samples of wild-type, Ctsb(-/-), and Ctsl(-/-) mice via mass-spectrometry-based proteomics. Both protease deficiencies revealed distinct quantitative changes in proteome composition. Ctsl(-/-) skin revealed increased levels of the cysteine protease inhibitors cystatin B and cystatin M/E, increased cathepsin D, and an accumulation of the extracellular glycoprotein periostin. Immunohistochemistry located periostin predominantly in the hypodermal connective tissue of Ctsl(-/-) skin. The proteomic identification of proteolytic cleavage sites within skin proteins revealed numerous processing sites that are underrepresented in Ctsl(-/-) or Ctsb(-/-) samples. Notably, few of the affected cleavage sites shared the canonical Ctsl or Ctsb specificity, providing further evidence of a complex proteolytic network in the skin. Novel processing sites in proteins such as dermokine and Notch-1 were detected. Simultaneous analysis of acetylated protein N termini showed prototypical mammalian N-alpha acetylation. These results illustrate an influence of both Ctsb and Ctsl on the murine skin proteome and degradome, with the phenotypic consequences of the absence of either protease differing considerably. Molecular & Cellular Proteomics 12: 10.1074/mcp.M112.017962, 611-625, 2013.

Characterization of PTZ-Induced Seizure Susceptibility in a Down Syndrome Mouse Model That Overexpresses CSTB

PLOS ONE

Authors: Brault, Veronique; Martin, Benoit; Costet, Nathalie; Bizot, Jean-Charles; Herault, Yann

Abstract

Down syndrome (DS) is a complex genetic syndrome characterized by intellectual disability, dysmorphism and variable additional physiological traits. Current research progress has begun to decipher the neural mechanisms underlying cognitive impairment, leading to new therapeutic perspectives. Pentylenetetrazol (PTZ) has recently been found to have positive effects on learning and memory capacities of a DS mouse model and is foreseen to treat DS patients. But PTZ is also known to be a convulsant drug at higher dose and DS persons are more prone to epileptic seizures than the general population. This raises concerns over what long-term effects of treatment might be in the DS population. The cause of increased propensity for epilepsy in the DS population and which Hsa21 gene(s) are implicated remain unknown. Among Hsa21 candidate genes in epilepsy, CSTB, coding for the cystein protease inhibitor cystatin B, is involved in progressive myoclonus epilepsy and ataxia in both mice and human. Thus we aim to evaluate the effect of an increase in Cstb gene dosage on spontaneous epileptic activity and susceptibility to PTZ-induced seizure. To this end we generated a new mouse model trisomic for Cstb by homologous recombination. We verified that increasing copy number of Cstb from Trisomy (Ts) to Tetrasomy (Tt) was driving overexpression of the gene in the brain, we checked transgenic animals for presence of locomotor activity and electroencephalogram (EEG) abnormalities characteristic of myoclonic epilepsy and we tested if those animals were prone to PTZ-induced seizure. Overall, the results of the analysis shows that an increase in Cstb does not induce any spontaneous epileptic activity and neither increase or decrease the propensity of Ts and Tt mice to myoclonic seizures suggesting that Ctsb dosage should not interfere with PTZ-treatment.