#NFkappaB
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docdellaire.bsky.social
The lack of senescence in their model might suggest TBK1-IKK-NFkappaB signaling is perhaps not functioning the same way as other tissues. For example STING can be potently activated in lung cancer by loss of Rb - see: pmc.ncbi.nlm.nih.gov/articles/PMC...
Mutant RB1 enhances therapeutic efficacy of PARPis in lung adenocarcinoma by triggering the cGAS/STING pathway
Poly (ADP-ribose) polymerase inhibitors (PARPis) are approved for cancer therapy according to their synthetic lethal interactions, and clinical trials have been applied in non–small cell lung cancer. ...
pmc.ncbi.nlm.nih.gov
July 27, 2025 at 8:32 PM
acr-journals.bsky.social
The ever-expanding connections between PAD4 and rheumatoid arthritis

Editorial on the below study in A&R
doi.org/10.1002/art....

Figure: Multiple roles of PAD4 in RA pathogenesis

#Medsky #Immunosky #Rheumsky
Multiple roles of PAD4 in RA pathogenesis. A. PAD4 in neutrophils citrullinates histones as part of NETosis and also citrullinates NFkappaB p65, leading to production of TNFa and IL-1β, which have inflammatory effects on many types of immune cells. Antigens in NETs are recognized by B cells that become ACPA-producing plasma cells. B. As newly described in Won et al, anti-PAD4 antibodies bind to monocytes, inducing IL-8, MCP-1, and MIP-1β, which recruit and activate neutrophils, monocytes, and lymphocytes. The T cells produce TNFa, IFNg, and IL-17, which stimulate synovial fibroblasts and provide help to B cells. C. In macrophages, PAD4 citrullinates histones enabling METosis. Like NETs, METs are recognized by B cells that will differentiate into plasma cells that secrete ACPAs. Figure created in BioRender
April 5, 2025 at 9:44 PM
alicefrolov.bsky.social
New visualization: The Senescence-Associated Secretory Phenotype Amplifies Over Time

I am sharing a figure developed to illustrate the temporal dynamics of SASP factor secretion following senescence induction.

#CellularSenescence #SASP #Inflammaging #Fibroblasts #NFkappaB
New visualization: The Senescence-Associated Secretory Phenotype Amplifies Over Time I am sharing a figure developed to illustrate the temporal dynamics of SASP factor secretion following senescence induction in human fibroblasts. The plot depicts simulated secretion trajectories of several canonical SASP components across a post-induction time course. I want to state explicitly at the outset that the data presented are simulated. They are not derived from a specific experimental dataset but instead constructed to reflect a literature-grounded consensus regarding the qualitative kinetics and relative temporal ordering of SASP factor release. The figure is intended as a didactic and conceptual reference rather than as an empirical result. The multiline plot tracks relative secretion levels of representative factors, including IL-6, IL-8, IL-1alpha, CXCL1/GROalpha, and MMP-3, over an extended interval following an initiating stress (e.g., oncogene activation, genotoxic insult, or replicative exhaustion). Several features are worth noting for peer discussion. First, the trajectories emphasize the non-immediate onset of the secretory program. Rather than accompanying cell cycle arrest instantaneously, robust SASP secretion emerges over a delayed window consistent with the established requirement for sustained DNA damage response signaling and the progressive activation of transcriptional regulators, notably NF-kappaB and C/EBPbeta. The kinetics reflect the intermediary role of the mTOR pathway and the ATM/GATA4 axis in stabilizing the secretory phenotype. Second, the curves illustrate the amplifying, self-reinforcing character of the phenotype. IL-1alpha is positioned as an upstream, membrane-associated signaling node driving downstream IL-6 and IL-8 expression through autocrine and paracrine feedforward loops.
July 14, 2026 at 5:00 PM
fly-broadcast.bsky.social
Neuron-specific suppression of aberrantly active Toll-NFkappaB signalling mitigates pathogenic tau hyperphosphorylation via Gsk-3beta in Drosophila
#Drosophila
Neuron-specific suppression of aberrantly active Toll-NFkappaB signalling mitigates pathogenic tau hyperphosphorylation via Gsk-3beta in Drosophila #Drosophila
PubMed link
pubmed.ncbi.nlm.nih.gov
August 4, 2026 at 5:23 AM
husslook.bsky.social
#kiss1 #suppresses #TNFalpha #breastcancer #cell #invasion #inhibition #NFkappaB #genetic #Houston #Texas

husslook.tumblr.com/post/534252637…
KiSS1 suppresses TNFalpha-induced breast cancer cell invasion via an inhibition of RhoA-mediated NF-kappaB activation.
t.co
April 5, 2025 at 10:30 PM
peiferlabunc.bsky.social
Cool work though it is a bit sad they have to call it NFkappaB signaling.... Yo Cell, its dorsal or its paralog
June 3, 2024 at 11:24 PM
biorxiv-biochem.bsky.social
Pirin does not bind to p65 or regulate NFkappaB-dependent gene expression https://www.biorxiv.org/content/10.1101/2024.12.03.626411v1
Pirin does not bind to p65 or regulate NFkappaB-dependent gene expression https://www.biorxiv.org/content/10.1101/2024.12.03.626411v1
Pirin is a non-heme iron binding protein with a variety of proposed functions including serving as a
www.biorxiv.org
December 4, 2024 at 1:46 PM
biorxivpreprint.bsky.social
Pirin does not bind to p65 or regulate NFkappaB-dependent gene expression https://www.biorxiv.org/content/10.1101/2024.12.03.626411v1
Pirin does not bind to p65 or regulate NFkappaB-dependent gene expression https://www.biorxiv.org/content/10.1101/2024.12.03.626411v1
Pirin is a non-heme iron binding protein with a variety of proposed functions including serving as a
www.biorxiv.org
December 4, 2024 at 1:46 PM
interactivefly.bsky.social
O'Hara, M. K., Saul, C., Handa, A., Sehgal, A., Williams, J. A. (2023). The NFkappaB Dif is required for behavioral and molecular correlates of sleep homeostasis in Drosophila. bioRxiv, www.biorxiv.org/content/10.1...
July 9, 2024 at 11:04 PM