Tnfr1 and Tnfr2 engage disparate survival signals.

The ability to discern between survival and immune effectors signals in signal transduction systems is a basic question. Generic depletion of TNFR2 activated Caspase-4 while silencing Caspase-9. Cells lacking TNFR2 further activated CARD8 and the CASP8 and FADD-like apoptosis regulator CFLAR. Using proteomics, we demonstrate selective interaction between TNFRSF1A and TANK/TBK1. Together we demonstrate here in human cells the ability of the TNF receptors Tnfr1 and Tnfr2 to engage disparate survival signals.

Authors

Publication Details

Journal
Zenodo (CERN European Organization for Nuclear Research)
Published
2026-11-02
DOI
https://doi.org/10.5281/zenodo.23891354
Primary Topic
Cell death mechanisms and regulation
Type
preprint
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preprint

Tnfr1 and Tnfr2 engage disparate survival signals.

Shahan Mamoor
Zenodo (CERN European Organization for Nuclear Research)
Cell death mechanisms and regulation
preprint

Tnfr1 and Tnfr2 engage disparate survival signals.

Shahan Mamoor
preprint en

Abstract

The ability to discern between survival and immune effectors signals in signal transduction systems is a basic question. Generic depletion of TNFR2 activated Caspase-4 while silencing Caspase-9. Cells lacking TNFR2 further activated CARD8 and the CASP8 and FADD-like apoptosis regulator CFLAR. Using proteomics, we demonstrate selective interaction between TNFRSF1A and TANK/TBK1. Together we demonstrate here in human cells the ability of the TNF receptors Tnfr1 and Tnfr2 to engage disparate survival signals.

Zenodo (CERN European Organization for Nuclear Research)
Good health and well-being
Cell death mechanisms and regulation
DOIOpen Access PDFOpenAlex
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Tnfr1 and Tnfr2 engage disparate survival signals. — Shahan Mamoor · Zenodo (CERN European Organization for Nuclear Research) (2026) | TGRS Research Map | TGRS