Top Tweets for #stat5
@houndcl @Andre_AGTC I have written about these #STAT6 independent pathways several times. #STAT5 via IL-2 can take up the mantle and play a key role as well, but IL-13 still blocked.
MAPK, PI3K
https://t.co/v9M5iXkbll
IL-2/STAT5
https://t.co/bpICGbK4ki
IL-6/STAT3, Th17
https://t.co/b7IUsyz4rL
In absence of IL-4Rα/#STAT6, #IL2 activated #STAT5 can act in a compensatory fashion to differentiate/activate/maintain #Th2 inflammation + activate production of pro-inflammatory cytokines: #IL4 #IL5 #IL13
Papers:
https://t.co/oDcHYK97qL
https://t.co/daBq3tOK7m
Pathway contributions to Th2 inflammation is very important consideration when assessing potential for #STAT6 degrader/inhibitors and bios in the space:
$KYMR $JNJ $GILD $SNY $NRIX Leo Kaken DeepCure
Pathways contributing to Th2 inflammation (AD and asthma) can be crudely estimated based on literature from gene expression profiling, KO mouse models, and functional studies.
Data shows >80% of IL-4-regulated genes being #STAT6-mediated, ~50% residual IL-4 production in STAT6-deficient T cells, and >90% reductions in eosinophilia/AHR/IgE in STAT6 KO allergic models.
Overall, the STAT6 pathway dominates transcriptional responses and effector outcomes, but independent arms (PI3K for proliferation, MAPK for amplification) provide ~20-30% support, sustaining residual activity in STAT6 absence.
How Can We Make Cancer-Fighting T cells Stronger and Longer-Lasting? - @PatrickHwuMD
@SciImmunology
https://t.co/dF217dnBz6
#OncoDaily #Oncology #Cancer #Health #Medicine #MedTwitter #MedEd #MedOnc #MedNews #Tcells #STAT5 #ScienceImmunology @CancerWorldmag
Scientists have engineered a viral protein that can harness LCK kinase to activate #STAT5 and sustain cytotoxic T cell activity within tumors in mice. @UMPharmacology
Read more in Science #Immunology: https://t.co/x0YMELyr56
Today: Sanofi announced it will pay Teva $500M upfront to co-develop and co-commercialize Teva’s anti-TL1A.
Rewind: Evercore ISI's Umer Raffat said during a July episode of Analyst Thursdays that he was surprised Teva was getting no credit for this asset back then.
@Interasma ITK required for #Th9 cells and IL-9. ITK deficiency or ITK inhibition leads to reduced #STAT5 #S6 #IRF4 #IL9 and Th9. Even in presence of #TL1A, cells fail to express IL-9 if ITK-deficient!
$CRVS oral ITK inhibitor #soquelitinib potential #IBD #asthma
https://t.co/PHAngtdxq4
@LabWaggoner @statfourwork @MucosalImmunol Even in presence of #TL1A, without #ITK, #STAT5 cannot bind to #IRF4 or #IL9 promoter genes.
Effects confirmed w/ old ITK inhibitor BMS-509744.
$CRVS oral ITK inhibitor #soquelitinib highly-selective. #Th9 #IL9 diseases #atopicdermatitis #asthma #IBD
https://t.co/rCY8I5nTwG
@LabWaggoner @statfourwork @MucosalImmunol Even in presence of #TL1A, without #ITK, #STAT5 cannot bind to #IRF4 or #IL9 promoter genes.
Effects confirmed w/ old ITK inhibitor BMS-509744.
$CRVS oral ITK inhibitor #soquelitinib highly-selective. #Th9 #IL9 diseases #atopicdermatitis #asthma #IBD
https://t.co/rCY8I5nTwG
@LabWaggoner @statfourwork @MucosalImmunol Even in presence of #TL1A, without #ITK, #STAT5 cannot bind to #IRF4 or #IL9 promoter genes.
Effects confirmed w/ old ITK inhibitor BMS-509744.
$CRVS oral ITK inhibitor #soquelitinib highly-selective. #Th9 #IL9 diseases #atopicdermatitis #asthma #IBD
https://t.co/rCY8I5nTwG
@LabWaggoner @statfourwork @MucosalImmunol Even in presence of #TL1A, without #ITK, #STAT5 cannot bind to #IRF4 or #IL9 promoter genes.
Effects confirmed w/ old ITK inhibitor BMS-509744.
$CRVS oral ITK inhibitor #soquelitinib highly-selective. #Th9 #IL9 diseases #atopicdermatitis #asthma #IBD
https://t.co/rCY8I5nTwG
@MucosalImmunol @statfourwork Even in presence of #TL1A, without #ITK, #STAT5 cannot bind to #IRF4 or #IL9 promoter genes.
Effects confirmed w/ old ITK inhibitor BMS-509744.
$CRVS oral ITK inhibitor #soquelitinib highly-selective. #Th9 #IL9 diseases #atopicdermatitis #asthma #IBD
https://t.co/rCY8I5orme
@LabWaggoner @statfourwork @MucosalImmunol Even in presence of #TL1A, without #ITK, #STAT5 cannot bind to #IRF4 or #IL9 promoter genes.
Effects confirmed w/ old ITK inhibitor BMS-509744.
$CRVS oral ITK inhibitor #soquelitinib highly-selective. #Th9 #IL9 diseases #atopicdermatitis #asthma #IBD
https://t.co/rCY8I5nTwG
@LabWaggoner @statfourwork @MucosalImmunol ITK supercedes this, required for #Th9 cells. ITK deficiency or ITK inhibition leads to reduced #STAT5 #S6 #IRF4 #IL9 and Th9.
Even in presence of #TL1A, cells fail to express IL-9 if ITK-deficient.
$CRVS oral ITK inhibitor #soquelitinib in #IBD #asthma
https://t.co/rCY8I5nTwG
@statfourwork ITK supercedes this, required for #Th9 cells. ITK deficiency or ITK inhibition leads to reduced #STAT5 #S6 #IRF4 #IL9 and Th9.
Even in presence of #TL1A, cells fail to express IL-9 if ITK-deficient.
$CRVS oral ITK inhibitor #soquelitinib in #IBD #asthma
https://t.co/rCY8I5nTwG
@MucosalImmunol @statfourwork ITK supercedes this, required for #Th9 / IL-9. ITK deficiency or ITK inhibition leads to reduced #STAT5 #S6 #IRF4 #IL9 and Th9.
Even in presence of #TL1A, cells fail to express IL-9 if ITK-deficient!
$CRVS oral ITK inhibitor #soquelitinib in #IBD #asthma
https://t.co/rCY8I5nTwG
@biorxiv_immuno ITK supercedes this and required for #Th9 + IL-9. ITK deficiency or ITK inhibition leads to reduced #STAT5 #S6 #IRF4 #IL9 and Th9.
Even in presence of #TL1A, cells fail to express IL-9 if ITK-deficient!
$CRVS oral ITK inhibitor #soquelitinib #asthma #IBD
https://t.co/rCY8I5nTwG
Excited to share our latest work with the #JAKSTAT research network led by @richard_moriggl @VetmeduniVienna in @jclinicalinvest! We show that hyperactive #STAT5 mimics TCR signaling in T-ALL, identifying STAT3/5 degraders & ZAP70 inhibitors as a synergistic therapeutic strategy!
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