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Gene Information
Gene symbol: MYD88
Gene name: myeloid differentiation primary response 88
HGNC ID: 7562
Related Genes
| # | Gene Symbol | Number of hits |
| 1 | HOXA3 | 1 hits |
| 2 | IL1B | 1 hits |
| 3 | INS | 1 hits |
| 4 | IRAK1 | 1 hits |
| 5 | LEP | 1 hits |
| 6 | NFKB1 | 1 hits |
| 7 | TICAM1 | 1 hits |
| 8 | TLR2 | 1 hits |
| 9 | TLR4 | 1 hits |
| 10 | TRIM69 | 1 hits |
Related Sentences
| # | PMID | Sentence |
| 1 | 10967106 | We show that overexpression of the Toll domain or the lpr mutant of MyD88 in betaTc-Tet cells decreased nuclear factor kappaB (NF-kappaB) activation upon IL-1beta and IL-1beta/interferon (IFN)-gamma stimulation. |
| 2 | 10967106 | Furthermore, our data show that IL-1beta cellular actions can be blocked by expression of MyD88 dominant negative proteins and, finally, that cytokine-induced beta cell secretory dysfunctions are due to the action of IFN-gamma. |
| 3 | 19544454 | Microarray analyses of HOXA3-treated wounds revealed that indeed HOXA3 locally increased expression of genes that selectively promote stem/progenitor cell mobilization and recruitment while also suppressing expression of numerous members of the proinflammatory nuclear factor kappaB pathway, including myeloid differentiation primary response gene 88 and toll-interacting protein. |
| 4 | 20733560 | Wounds of TLR2(-/-)+STZ mice showed less oxidative stress, decreased MyD88 signaling, NF-?B activation, and cytokine secretion. |
| 5 | 20824098 | In the present study, we found MyD88-deficient mice fed a HFD had increased circulating levels of insulin, leptin and cholesterol, as well as liver dysfunction (increased induction of ALT levels, increased activation of JNK and cleavage of PARP), which were linked to the onset of severe diabetes. |
| 6 | 20067962 | Type 2 diabetic subjects showed increased MyD88, phosphorylated IRAK-1, Trif, TICAM-1, IRF-3, and NF-kappaB p65 expression in monocytes compared with control subjects. |
| 7 | 21498084 | Also, levels of MyD88, IRAK-1 protein phosphorylation, Trif, IRF3, and NF-?B activity were significantly reduced in TLR4(-/-) +STZ mice compared to the WT+STZ mice. |