Human CILP blocking peptide

Name: Human CILP blocking peptide
SKU: CDBP0807
Rating: 5 (1 reviews)

Synthetic Human CILP blocking peptide for Apuri, BL, ELISA

COA

SDS

Datasheet

Summary

Product Overview

Blocking/Immunizing peptide for anti-CILP antibody

Target

CILP

Nature

Synthetic

Tag/Conjugate

Unconjugated

Application Notes

For in vitro research use only. Not intended for any diagnostic or therapeutic purpose. Not for human or animal consumption.

Format

Lyophilized powder

Preservative

None

Storage

Shipped at ambient temperature, store at -20°C.

Entrez Gene ID

8483

Antigen Description

Major alterations in the composition of the cartilage extracellular matrix occur in joint disease, such as osteoarthrosis. This gene encodes the cartilage intermediate layer protein (CILP), which increases in early osteoarthrosis cartilage. The encoded protein was thought to encode a protein precursor for two different proteins; an N-terminal CILP and a C-terminal homolog of NTPPHase, however, later studies identified no nucleotide pyrophosphatase phosphodiesterase (NPP) activity. The full-length and the N-terminal domain of this protein was shown to function as an IGF-1 antagonist. An allelic variant of this gene has been associated with lumbar disc disease.

Function

NOT alkaline phosphatase activity; NOT nucleotide diphosphatase activity;

Synonyms

CILP; cartilage intermediate layer protein, nucleotide pyrophosphohydrolase; cartilage intermediate layer protein 1; HsT18872; cartilage intermediate-layer protein; cartilage intermediate layer protein 1 C1; cartilage intermediate layer protein 1 C2; CILP-1;

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Functional polymorphisms in asporin and CILP together with joint loading predispose to hand osteoarthritis

BMC GENETICS

Authors: Taipale, Mari; Solovieva, Svetlana; Leino-Arjas, Paivi; Mannikko, Minna

Abstract

Background: Osteoarthritis (OA) is the most common degenerative joint disease afflicting people in the Western world and has a strong genetic influence. The aim of this study was to examine the association of two known functional polymorphisms in the TGF-beta inhibiting genes, asporin (ASPN) and cartilage intermediate layer protein (CILP), with hand OA and potential gene-occupational hand loading interaction. Results: Statistically significant interaction of the CILP rs2073711 T and ASPN D15 alleles with hand OA was observed (OR = 2.48, 95% CI 1.27-4.85, p = 0.008) in a Finnish hand. OA cohort of 543 women (aged. 45-63). When stratified by variation in working tasks, low variation of working tasks increased the risk further (OR = 3.00, 95% CI 1.35-6.66, p = 0. 007). Based on the analysis of ASPN and CILP protein-coding regions, functional studies were performed with one observed variant, rs41278695 in the ASPN 'gene. Analyses showed that bone morphogenetic protein 2 (BMP2) mediated expression of aggrecan (Agc1) and type II collagen (Col2a1) was significantly suppressed (p = 0.011 and p = 0.023, respectively) in a murine chondrocytic cell line (ATDC5) with cells stably expressing ASPN rs41278695. Conclusions: The carriage of either ASPN D15 or CILP rs2073711 TT is associated, with increased risk of symmetrical hand. OA, particularly in individuals with low variation in work tasks. ASPN rs41278695 SNP had an effect on Agc1 and. Col2a1 gene expression when induced with BMP-2 suggesting an effect on the cartilage extracellular matrix composition.

Mice depleted of alpha beta but not gamma delta T cells are resistant to mortality caused by cecal ligation and puncture

SHOCK

Authors: Enoh, Victor T.; Lin, Scott H.; Lin, Cheng Y.; Toliver-Kinsky, Tracy; Murphey, Erle D.; Varma, Tushar K.; Sherwood, Edward R.

Abstract

The present study was undertaken to determine whether the mice depleted of alpha beta or gamma delta T cells show resistance to acute polymicrobial sepsis caused by cecal ligation and puncture (CLIP). T-cell receptor beta knockout (beta TCRKO) and T-cell receptor delta knockout (delta TCRKO) mice were used. An additional group of mice was treated with an antibody against the alpha beta T-cell receptor to induce alpha beta T-cell depletion; a subset of alpha beta T cell-deficient mice was also treated with anti-asialoGM1 to deplete natural killer (NK) cells. The mice underwent CILP and were monitored for survival, temperature, acid-base balance, bacterial counts, and cytokine production. The beta TCRKO mice and the wild-type mice treated with anti-P T-cell receptor (anti-TCR beta) antibody showed improved survival after CLP compared with wild-type mice. The treatment of alpha beta T cell-deficient mice with anti-asialoGM1 further improved survival after CLP, especially when the mice were treated with imipenem. The improved survival observed in alpha beta T cell-deficient mice was associated with less hypothermia, improved acid-base balance, and decreased production of the proinflammatory cytokines interleukin (IL) 6 and macrophage inflammatory protein (MIP) 2. Compared with wild-type controls, the overall survival was not improved in delta TCRKO mice. The concentrations of IL-6 and MIP-2 in plasma and cytokine mRNA expression in tissues were not significantly different between wild-type and delta TCRKO mice. These studies indicate that mice depleted of alpha beta but not of gamma delta T cells are resistant to mortality in an acutely lethal model of CLP. The depletion of NK cells caused further survival benefit in alpha beta T cell-deficient mice. These findings suggest that alpha beta T and NK cells mediate or facilitate CLP-induced inflammatory injury.