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Inflammatory Immune Response Articles & Analysis

3 articles found

Has the future of complement therapeutics arrived?   

Has the future of complement therapeutics arrived?  

Silence Therapeutics, a pioneer in the development of novel small interfering RNA (siRNA) therapeutics, and Mallinckrodt plc, a global biopharmaceutical company, announced the submission of a clinical trial application (CTA) for SLN501, a siRNA therapy targeting the complement C3 protein, on March 23, 2022. Silence will receive a $3 million milestone payment from Mallinckrodt as a result of the ...

ByCreative Biolabs


RelB Modulation of Ikappa Balpha Stability as a Mechanism of Transcription Suppression of Interleukin-1alpha (IL-1alpha ), IL-1beta , and Tumor Necrosis Factor Alpha in Fibroblasts

RelB Modulation of Ikappa Balpha Stability as a Mechanism of Transcription Suppression of Interleukin-1alpha (IL-1alpha ), IL-1beta , and Tumor Necrosis Factor Alpha in Fibroblasts

Members of the NF-B/RelB family of transcription factors play important roles in the regulation of inflammatory and immune responses. RelB, a member of this family, has been characterized as a transcription activator and is involved in the constitutive NF-B activity in lymphoid tissues. However, in a previous study we observed an overexpression of chemokines in RelB-deficient fibroblasts. Here we ...

ByAmerican Society for Microbiology (ASM)


Relb modulation of ib stability as a mechanism of transcription suppression of interleukin-1 (il-1), il-1, and tumor necrosis factor alpha in fibroblasts

Relb modulation of ib stability as a mechanism of transcription suppression of interleukin-1 (il-1), il-1, and tumor necrosis factor alpha in fibroblasts

Members of the NF-B/RelB family of transcription factors play important roles in the regulation of inflammatory and immune responses. RelB, a member of this family, has been characterized as a transcription activator and is involved in the constitutive NF-B activity in lymphoid tissues. However, in a previous study we observed an overexpression of chemokines in RelB-deficient fibroblasts. Here we ...

ByAmerican Society for Microbiology (ASM)

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