IndraLab

Statements


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"However, our data indicate that this dysregulation can be further driven by TNFAIP3 loss in patients with MYD88 mutations.The importance of IL-6 and the autocrine mechanism by which IL-6 induces STAT3 activation in DLBCL has been shown in previous studies ."

sparser
"We found that A20 can simultaneously inhibit MyD88 and TBK1 signals by binding Nrdp1, suggesting that Nrdp1 plays a key role in A20-mediated regulation of inflammatory signals."

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"Loss of TNFAIP3 enhances MYD88 -driven signaling in non-Hodgkin lymphoma, presenting a potential opportunity for therapeutic targeting (59)."

reach
"Using the MWCL-A20 and HBL-1-A20 , we were able to show that loss of TNFAIP3 enhances MYD88 -driven NF-κB and p38 signaling resulting in increased expression of NF-κB target genes IL-6 and CXCL10, known NF-κB target genes , have both been shown to be significantly upregulated in WM and DLBCL, and higher serum levels correlate with an inferior survival ."