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Recombinant Rat Myeloid differentiation primary response protein MyD88 (Myd88)

Recombinant Rat Myeloid differentiation primary response protein MyD88 (Myd88)

Code
MSDS	MSDS Datasheet
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Source
Conjugate
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Product Details
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Target Background

Product Details

Abbreviation

Myd88

Purity

>85% (SDS-PAGE)

Target Names

Myd88

Uniprot NO.

Q6Y1S1

Alternative Names

Myd88; Myeloid differentiation primary response protein MyD88

Species

Rattus norvegicus (Rat)

Source

Yeast

Expression Region

1-296

Target Protein Sequence

MSAGGPRVGS VSVDSYLFSL PLVALNVGVR RRLSLFLNPR TTAAADWTSL AEEMGFEYLE IREFETRPDP TRSLLDAWQG RSGSSVGRLL ELLALLDRED ILYELKDRIE EDCQKYIRNQ QKQESEKPLQ VARVESSVPQ TKELGGITTL DDPLGQTPEL FDAFICYCPS DIEFVQEMIR QLEQTDYRLK LCVSDRDVLP GTCVWSIASE LIEKRCRRMV VVVSDDYLQS KECDFQTKFA LSLSPGVQQK RLIPIKYKAM KKDFPSILRF ITICDYTNPC TKSWFWTRLA KALSLP
Note: The complete sequence may include tag sequence, target protein sequence, linker sequence and extra sequence that is translated with the protein sequence for the purpose(s) of secretion, stability, solubility, etc.
If the exact amino acid sequence of this recombinant protein is critical to your application, please explicitly request the full and complete sequence of this protein before ordering.

Protein Length

full length protein

Tag Info

N-terminal His-tagged/Tag-Free
The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.

Storage Condition

The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.

Shelf Life

Notes

Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.

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Target Background

Function(From Uniprot)

Adapter protein involved in the Toll-like receptor and IL-1 receptor signaling pathway in the innate immune response. Acts via IRAK1, IRAK2, IRF7 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Increases IL-8 transcription. Involved in IL-18-mediated signaling pathway. Activates IRF1 resulting in its rapid migration into the nucleus to mediate an efficient induction of IFN-beta, NOS2/INOS, and IL12A genes. Upon TLR8 activation by GU-rich single-stranded RNA (GU-rich RNA) derived from viruses, induces IL1B release through NLRP3 inflammasome activation. MyD88-mediated signaling in intestinal epithelial cells is crucial for maintenance of gut homeostasis and controls the expression of the antimicrobial lectin REG3G in the small intestine.

Gene References into Functions

n-3 PUFAs may reduce acute RE in rats, which may be due to inhibition of the MyD88-NF-kB pathway and limit oxidative damage. PMID:27716366
this study shows that Myd88 expression is up-regulated in experimental periodontitis PMID:27107801
Results suggest that the myeloid differentiation factor 88 (MyD88) pathway plays a critical role in their immune defense activity. PMID:26684858
High MYD88 expression is associated with corneal allograft rejection after penetrating keratoplasty. PMID:25800037
Cardiac RNA induces inflammatory responses in cardiomyocytes and immune cells via MyD88-TLR7 signaling. PMID:26363072
The study aims to detect the expression level of MyD88 and know more about the role of MyD88 after Subarachnoid hemorrhage PMID:23684713
Myd88 is increasingly expressed in a parallel time course to the up-regulation of nuclear factor-kappaB, proinflammatory cytokines and ICAM-1; there is a highly positive relationship among them. PMID:21530945
disruption of MyD88 or TRIF signaling does not confer protection in brain ischemia PMID:21376021
Intrauterine LPS infusion can induce an increased expression levels of TLR4 and MyD88 in the lung PMID:20021788
Our results suggest that MyD88 is an important component in the Toll-like receptor-4-mediated nuclear factor-kappaB activation pathway that contributes to the development of cardiac hypertrophy. PMID:16199478
The results demonstrate that both inhibition of the NFkappaB activation pathway and activation of the Akt signaling pathway may be responsible for the protective effect of transfection of dominant negative MyD88. PMID:16259957
Absence of MyD88 enhances the tolerogenicity of dendritic cells (DCs) and suggest that inhibiting innate immunity may be a potential strategy to facilitate induction of transplant tolerance by DCs. PMID:18589162
Results suggest that Der p2 activates the MyD88 signaling pathway through toll-like receptor (TLR) 2, and induces asthma through the MyD88 signaling pathway in respiratory tissue. PMID:19326394
Myd88-dependent Nf-kB activation is involved in fibrinogen-induced hyperrophic response of cardiomyocytes. PMID:19342961