Human NLRP3 blocking peptide

Name: Human NLRP3 blocking peptide
SKU: CDBP0802
Rating: 5 (1 reviews)

Synthetic Human NLRP3 blocking peptide for Apuri, BL, ELISA

COA

SDS

Datasheet

Summary

Product Overview

Blocking/Immunizing peptide for anti-CIAS1/Cryopyrin (Internal) antibody

Target

CIAS1 / Cryopyrin (Internal)

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

114548

Antigen Description

This gene encodes a pyrin-like protein containing a pyrin domain, a nucleotide-binding site (NBS) domain, and a leucine-rich repeat (LRR) motif. This protein interacts with the apoptosis-associated speck-like protein PYCARD/ASC, which contains a caspase recruitment domain, and is a member of the NALP3 inflammasome complex. This complex functions as an upstream activator of NF-kappaB signaling, and it plays a role in the regulation of inflammation, the immune response, and apoptosis. Mutations in this gene are associated with familial cold autoinflammatory syndrome (FCAS), Muckle-Wells syndrome (MWS), chronic infantile neurological cutaneous and articular (CINCA) syndrome, and neonatal-onset multisystem inflammatory disease (NOMID). Multiple alternatively spliced transcript variants encoding distinct isoforms have been identified for this gene. Alternative 5' UTR structures are suggested by available data; however, insufficient evidence is available to determine if all of the represented 5' UTR splice patterns are biologically valid. [provided by RefSeq, Oct 2008]

Function

ATP binding; peptidoglycan binding; protein binding;

Synonyms

NLRP3; NLR family, pyrin domain containing 3; AII; AVP; FCU; MWS; FCAS; CIAS1; NALP3; C1orf7; CLR1.1; PYPAF1; AGTAVPRL; NACHT, LRR and PYD domains-containing protein 3; cryopyrin; caterpiller protein 1.1; PYRIN-containing APAF1-like protein 1; NACHT, LRR and PYD containing protein 3; cold autoinflammatory syndrome 1 protein; NACHT domain-, leucine-rich repeat-, and PYD-containing protein 3; nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain containing 3;

Citations

Have you cited CDBP0802 in a publication? Let us know and earn a reward for your research.

Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Recent progress in therapeutic drug delivery systems for treatment of traumatic CNS injuries

FUTURE MEDICINAL CHEMISTRY

Authors: Khadka, Bikram; Lee, Jae-Young; Kim, Ki-Taek; Bae, Jong-Sup

Abstract

Most therapeutics for the treatment of traumatic central nervous system injuries, such as traumatic brain injury and spinal cord injury, encounter various obstacles in reaching the target tissue and exerting pharmacological effects, including physiological barriers like the blood-brain barrier and blood-spinal cord barrier, instability rapid elimination from the injured tissue or cerebrospinal fluid and off-target toxicity. For central nervous system delivery, nano- and microdrug delivery systems are regarded as the most suitable and promising carriers. In this review, the pathophysiology and biomarkers of traumatic central nervous system injuries (traumatic brain injury and spinal cord injur) are introduced. Furthermore, various drug delivery systems, novel combinatorial therapies and advanced therapies for the treatment of traumatic brain injury and spinal cord injur are emphasized.

Long non-coding RNA MEG3 inhibits M2 macrophage polarization by activating TRAF6 via microRNA-223 down-regulation in viral myocarditis

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE

Authors: Xue, Yu-Long; Zhang, Sheng-Xiao; Zheng, Chao-Feng; Li, Yu-Feng; Zhang, Li-Hui; Su, Qin-Yi; Hao, Yu-Fei; Wang, Shu; Li, Xue-Wen

Abstract

Viral myocarditis (VMC) commonly triggers heart failure, for which no specific treatments are available. This study aims to explore the specific role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) in VMC. A VMC mouse model was induced byCoxsackievirus B3(CVB3). Then, MEG3 and TNF receptor-associated factor 6 (TRAF6) were silenced and microRNA-223 (miR-223) was over-expressed in the VMC mice, followed by determination of ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS). Dual-luciferase reporter assay was introduced to test the interaction among MEG3, TRAF6 and miR-223. Macrophages were isolated from cardiac tissues and bone marrow, and polarization of M1 or M2 macrophages was induced. Then, the expressions of components of NLRP3 inflammatory body (NLRP3, ASC, Caspase-1), M1 markers (CD86, iNOS and TNF-alpha) and M2 markers (CD206, Arginase-1 and Fizz-1) were measured following MEG3 silencing. In the VMC mouse model, MEG3 and TRAF6 levels were obviously increased, while miR-223 expression was significantly reduced. Down-regulation of MEG3 resulted in the inhibition of TRAF6 by promoting miR-223. TRAF6 was negatively correlated with miR-223, but positively correlated with MEG3 expression. Down-regulations of MEG3 or TRAF6 or up-regulation of miR-223 was observed to increase mouse weight, survival rate, LVEF and LVFS, while inhibiting myocarditis and inflammationviathe NF-kappa B pathway inactivation in VMC mice. Down-regulation of MEG3 decreased M1 macrophage polarization and elevated M2 macrophage polarization by up-regulating miR-223. Collectively, down-regulation of MEG3 leads to the inhibition of inflammation and induces M2 macrophage polarizationviamiR-223/TRAF6/NF-kappa B axis, thus alleviating VMC.