Molecular Medicine - Journal
Article in Press: TGF-β1 signaling in Crohn’s disease | #MolecularMedicine #TGFbeta #CrohnsDisease link.springer.com/article/10.1...
Article in Press: TGF-β1 signaling in Crohn’s disease | #MolecularMedicine #TGFbeta #CrohnsDisease link.springer.com/article/10.1...
TGF-β1 signaling in Crohn’s disease - Molecular Medicine
Crohn's disease (CD), a chronic inflammatory disorder of the gastrointestinal tract, arises from the intricate interplay among genetic predisposition, environmental triggers, and gut microbial communi...
link.springer.com
September 23, 2026 at 3:37 PM
Molecular Medicine - Journal
Article in Press: TGF-β1 signaling in Crohn’s disease | #MolecularMedicine #TGFbeta #CrohnsDisease link.springer.com/article/10.1...
Article in Press: TGF-β1 signaling in Crohn’s disease | #MolecularMedicine #TGFbeta #CrohnsDisease link.springer.com/article/10.1...
Congratulations !🥳
It is super-intriguing to see a regenerating zone with quenched TGFbeta-signaling AND exacerbated fibrogenesis😎
It is super-intriguing to see a regenerating zone with quenched TGFbeta-signaling AND exacerbated fibrogenesis😎
September 11, 2026 at 5:35 PM
Congratulations !🥳
It is super-intriguing to see a regenerating zone with quenched TGFbeta-signaling AND exacerbated fibrogenesis😎
It is super-intriguing to see a regenerating zone with quenched TGFbeta-signaling AND exacerbated fibrogenesis😎
5/5 🥳Congratulations to PhD students Magali Miserocchi and Pauline De Meyer, who drove the study, and big thanks to our collaborators from the @stainierlab.bsky.social 🤩
#Microglia #Neuroimmunology #Zebrafish #DevelopmentalBiology #TGFbeta
#Microglia #Neuroimmunology #Zebrafish #DevelopmentalBiology #TGFbeta
August 25, 2026 at 6:52 PM
5/5 🥳Congratulations to PhD students Magali Miserocchi and Pauline De Meyer, who drove the study, and big thanks to our collaborators from the @stainierlab.bsky.social 🤩
#Microglia #Neuroimmunology #Zebrafish #DevelopmentalBiology #TGFbeta
#Microglia #Neuroimmunology #Zebrafish #DevelopmentalBiology #TGFbeta
Molecular Medicine-Article In Press: Human podocytes uniquely express CD47 to limit ITGAV-dependent TGF-β signaling for protection #Kidney #Podocytes #CD47 #TGFbeta link.springer.com/article/10.1...
August 24, 2026 at 3:33 PM
Molecular Medicine-Article In Press: Human podocytes uniquely express CD47 to limit ITGAV-dependent TGF-β signaling for protection #Kidney #Podocytes #CD47 #TGFbeta link.springer.com/article/10.1...
TIF1γ regulates stability of regulatory T cells during inflammation
->Nature | More on "Immune regulation and inflammatory response" at BigEarthData.ai
->Nature | More on "Immune regulation and inflammatory response" at BigEarthData.ai
TIF1γ regulates stability of regulatory T cells during inflammation
Yu, C. et al. The roles of TIF1γ in cancer. Front. Oncol. 9, 979 (2019). Dupont, S. et al. FAM/USP9x, a deubiquitinating enzyme essential for TGFbeta signaling, controls Smad4 monoubiquitination. Cell 136, 123–135 (2009). Quéré, R. et al. Tif1γ regulates the TGF-β 1 receptor and promotes physiological aging of hematopoietic stem cells. Proc. Natl Acad. Sci. USA 111, 10592–10597 (2014). Xue, J. et al. Tumour suppressor TRIM33 targets nuclear β-catenin degradation. Nat. Commun. 6, 6156 (2015). He, W. et al. Hematopoiesis controlled by distinct TIF1gamma and Smad4 branches of the TGFbeta pathway. Cell 125, 929–941 (2006). Chen, W. TGF-β regulation of T cells. Annu. Rev. Immunol. 41, 483–512 (2023). Tai, X. et al. How autoreactive thymocytes differentiate into regulatory versus effector CD4+ T cells after avoiding clonal deletion. Nat. Immunol. 24, 637–651 (2023). Chen, W. et al. Conversion of peripheral CD4+CD25- naive T cells to CD4+CD25+ regulatory T cells by TGF-beta induction of transcription factor Foxp3. J. Exp. Med. 198, 1875–1886 (2003). Rao, P. E., Petrone, A. L. & Ponath, P. D. Differentiation and expansion of T cells with regulatory function from human peripheral lymphocytes by stimulation in the presence of TGF-beta. J. Immunol. 174, 1446–1455 (2005). Moreau, J. M...
www.nature.com
August 11, 2026 at 8:16 PM
Tittelen er viktig, også i forskningsartikler. Får du ikke lyst til å lese revmatologi nå, så gjør du det aldri: <a href="http://www.ncbi.nlm.nih.gov/pubmed/16774692" class="hover:underline text-blue-600 dark:text-sky-400 no-card-link" target="_blank" rel="noopener" data-link="bsky">http://www.ncbi.nlm.nih.gov/pubmed/16774692
Scar wars: is TGFbeta the phantom menace in scleroderma? ...
The autoimmune disease scleroderma (systemic sclerosis (S...
www.ncbi.nlm.nih.gov
November 16, 2024 at 9:25 PM
Tittelen er viktig, også i forskningsartikler. Får du ikke lyst til å lese revmatologi nå, så gjør du det aldri: <a href="http://www.ncbi.nlm.nih.gov/pubmed/16774692" class="hover:underline text-blue-600 dark:text-sky-400 no-card-link" target="_blank" rel="noopener" data-link="bsky">http://www.ncbi.nlm.nih.gov/pubmed/16774692
Muscle-derived myostatin is a major endocrine driver of follicle-stimulating hormone synthesis | Science science.org/doi/10.1126/sc…. Major advance in endocrinology. So fascinating that new important hormonal actions of TGFBeta family members are still being discovered.
https://science.org/doi/10.1126/sc…
January 18, 2025 at 5:25 PM
Muscle-derived myostatin is a major endocrine driver of follicle-stimulating hormone synthesis | Science science.org/doi/10.1126/sc…. Major advance in endocrinology. So fascinating that new important hormonal actions of TGFBeta family members are still being discovered.
I like the approach of targeting both pathology and restoring dystrophin both with ASOs. However, I also wonder whether other ASO modalities (e.g. RNase H or siRNAs) might have been more effective. Then again, maybe too much reduction of TGFbeta might not be tolerated.
September 23, 2025 at 6:41 AM
I like the approach of targeting both pathology and restoring dystrophin both with ASOs. However, I also wonder whether other ASO modalities (e.g. RNase H or siRNAs) might have been more effective. Then again, maybe too much reduction of TGFbeta might not be tolerated.
However, this is not the same as chronic of course. Another thing I wonder about is whether long term treatment would be a problem, OR whether there would be a feedback mechanism where TGFbeta signaling is restored to normal levels (in our own hands in the past this is what we saw happening).
September 23, 2025 at 6:40 AM
However, this is not the same as chronic of course. Another thing I wonder about is whether long term treatment would be a problem, OR whether there would be a feedback mechanism where TGFbeta signaling is restored to normal levels (in our own hands in the past this is what we saw happening).
Furthermore, Duchenne patients have fibrosis, but also adipose tissue deposition and I do not know if the combination therapy would work as well there as in this mouse model. Authors discuss that chronically targeting TGFbeta signaling is not a good idea, due to its crucial role in many processes
September 23, 2025 at 6:38 AM
Furthermore, Duchenne patients have fibrosis, but also adipose tissue deposition and I do not know if the combination therapy would work as well there as in this mouse model. Authors discuss that chronically targeting TGFbeta signaling is not a good idea, due to its crucial role in many processes
They hypothesized that reducing TGFbeta with PMOs might be a good add-on therapy. They designed several PMOs to block TGFbeta transcript translation showing a decrease in TGFbeta production in cultured macrophages (stimulated with LPS).
September 23, 2025 at 6:31 AM
They hypothesized that reducing TGFbeta with PMOs might be a good add-on therapy. They designed several PMOs to block TGFbeta transcript translation showing a decrease in TGFbeta production in cultured macrophages (stimulated with LPS).
Authors used a fluorescent ASO to see where the PMO ended up, showing primarily localization at regenerating lesions, which there were less off in d2/mdx mice. They speculated that the increased TGFbeta signaling this model has played a role in reducing regeneration.
September 23, 2025 at 6:30 AM
Authors used a fluorescent ASO to see where the PMO ended up, showing primarily localization at regenerating lesions, which there were less off in d2/mdx mice. They speculated that the increased TGFbeta signaling this model has played a role in reducing regeneration.
authors present a rapid method to generate IPSCs that does not use viruses or recombinant proteins but a cocktail of: CHIR99021 (GSKinhibitor) PD0325901 (MEK inhibitor), SB431542 (TGFbeta activin nodal receptor inhibitor), Y-27632 (ROCK inhibitor), sodium butyrate, ascorbic acid & bFGF in ReproTESR
February 10, 2025 at 8:13 AM
authors present a rapid method to generate IPSCs that does not use viruses or recombinant proteins but a cocktail of: CHIR99021 (GSKinhibitor) PD0325901 (MEK inhibitor), SB431542 (TGFbeta activin nodal receptor inhibitor), Y-27632 (ROCK inhibitor), sodium butyrate, ascorbic acid & bFGF in ReproTESR
Today we had the priviledge of presenting the results from our #tgfbeta&cancer group @idibell.bsky.social #ciberehd to Prof. Natalie Törok @stanfordpress.bsky.social . Preliminary data from projects funded by #aecc_contraelcancer_es and #aei_micinn_es. Thanks,Natalie, for your inputs and advices!!!
May 29, 2025 at 3:52 PM
Today we had the priviledge of presenting the results from our #tgfbeta&cancer group @idibell.bsky.social #ciberehd to Prof. Natalie Törok @stanfordpress.bsky.social . Preliminary data from projects funded by #aecc_contraelcancer_es and #aei_micinn_es. Thanks,Natalie, for your inputs and advices!!!
Gli2 can be activated by canonical ligands like sonic hedgehog (Shh), or via noncanonical means (hypoxia/TGFbeta, VEGFc, alternative splicing, genetic mutations) This has led to failures of inhibitors of canonical hedgehog signaling which block Smoothened-Shh.
February 24, 2025 at 6:59 PM
Gli2 can be activated by canonical ligands like sonic hedgehog (Shh), or via noncanonical means (hypoxia/TGFbeta, VEGFc, alternative splicing, genetic mutations) This has led to failures of inhibitors of canonical hedgehog signaling which block Smoothened-Shh.
EMT can be induced by TGFbeta and hypoxia, is associated with therapeutic resistance to treatments like chemotherapy, targeted therapy, and immunotherapy. But the exact mechanisms leading to this resistance remain unknown. www.frontiersin.org/journals/imm...
February 24, 2025 at 6:58 PM
EMT can be induced by TGFbeta and hypoxia, is associated with therapeutic resistance to treatments like chemotherapy, targeted therapy, and immunotherapy. But the exact mechanisms leading to this resistance remain unknown. www.frontiersin.org/journals/imm...
#MysterySolved! Mashreghi Kallinich Goetzke &co show @nature.com that. children developing severe acute hyperinflammmatory shock after SARS-CoV-2 encounter (MIS-C) do so because of reactivation of EBV in B cells caused by excessive TGFbeta which impairs anti-EBV T memory cells!
TGFβ links EBV to multisystem inflammatory syndrome in children - Nature
Multisystem inflammatory syndrome following SARS-CoV-2 infection results from increased serum levels of TGFβ, which impairs the reactivation of virus-specific T cells.
doi.org
March 12, 2025 at 7:30 PM
#MysterySolved! Mashreghi Kallinich Goetzke &co show @nature.com that. children developing severe acute hyperinflammmatory shock after SARS-CoV-2 encounter (MIS-C) do so because of reactivation of EBV in B cells caused by excessive TGFbeta which impairs anti-EBV T memory cells!
🤜 A jujitsu move - turning suppressive TGFbeta in the TIME into IL-15 signaling for CARs DX.DOI.ORG/10.1016/j...
February 1, 2025 at 12:30 AM
🤜 A jujitsu move - turning suppressive TGFbeta in the TIME into IL-15 signaling for CARs DX.DOI.ORG/10.1016/j...
maybe due to mitotic defects and EMT? It's uncommon in WT MCF10A but can be enhanced by TGFbeta etc
www.cell.com/cell-reports...
www.cell.com/cell-reports...
Genomic Instability Is Induced by Persistent Proliferation of Cells Undergoing Epithelial-to-Mesenchymal Transition
The plasticity of EMT suggests that it is governed by reversible changes in gene expression.
Comaills et al. show that persistent proliferation of cells undergoing EMT, through
suppression of nuclear ...
www.cell.com
March 6, 2025 at 12:56 PM
maybe due to mitotic defects and EMT? It's uncommon in WT MCF10A but can be enhanced by TGFbeta etc
www.cell.com/cell-reports...
www.cell.com/cell-reports...
The May 2026 issue is out with exciting reviews on exercise-modulated microRNAs in skeletal muscle remodelling and TGFbeta signaling in chronic kidney injury
link.springer.com/journal/424/...
link.springer.com/journal/424/...
Pflügers Archiv - European Journal of Physiology
Pflügers ArchivEuropean Journal of Physiology is the official journal of the German Physiological Society, publishing high-quality original research in ...
link.springer.com
June 1, 2026 at 6:31 AM
The May 2026 issue is out with exciting reviews on exercise-modulated microRNAs in skeletal muscle remodelling and TGFbeta signaling in chronic kidney injury
link.springer.com/journal/424/...
link.springer.com/journal/424/...
He's Professor & for a long time was Dept Head at Genetics, cell & developmental Biology at U of Minnesota. TGFbeta & Steroid hormone signaling. A great scientist, mentor & leader. Another fun-fact--as a PhD student and postdoc he was a nationally ranked telemark skier
cbs.umn.edu/directory/mi...
cbs.umn.edu/directory/mi...
February 18, 2024 at 6:08 PM
He's Professor & for a long time was Dept Head at Genetics, cell & developmental Biology at U of Minnesota. TGFbeta & Steroid hormone signaling. A great scientist, mentor & leader. Another fun-fact--as a PhD student and postdoc he was a nationally ranked telemark skier
cbs.umn.edu/directory/mi...
cbs.umn.edu/directory/mi...
Not surprised with senescent cells, but netosis is exotic! Would have guessed TGFbeta/EMT/MMPs as the main culprit. Will read full paper, when at work, but I wonder if >cancer-relevant venetoclax or Pi3K/AKT inhibitors would be better than that basket of off-targets called dasatinib+quercetin
July 22, 2025 at 8:51 PM
Not surprised with senescent cells, but netosis is exotic! Would have guessed TGFbeta/EMT/MMPs as the main culprit. Will read full paper, when at work, but I wonder if >cancer-relevant venetoclax or Pi3K/AKT inhibitors would be better than that basket of off-targets called dasatinib+quercetin
#JiangsuHengruiPharma has chalked up a first-in-class approval for retlirafusp alfa, a #bifunctionaldrug that targets #PDL1 and #TGFbeta, as a treatment for advanced #gastriccancer.
pharmaphorum.com/news/hengrui...
pharmaphorum.com/news/hengrui...
January 8, 2026 at 12:52 PM
#JiangsuHengruiPharma has chalked up a first-in-class approval for retlirafusp alfa, a #bifunctionaldrug that targets #PDL1 and #TGFbeta, as a treatment for advanced #gastriccancer.
pharmaphorum.com/news/hengrui...
pharmaphorum.com/news/hengrui...
Very nice work! Inhibition of Hippo signaling, activation of Wnt signaling and TGFbeta signaling give rise to MTSC. J Zhang: Mouse trophectoderm stem cells generated with morula signalling inducers capture an
early trophectoderm state
early trophectoderm state
Mouse trophectoderm stem cells generated with morula signalling inducers capture an early trophectoderm state - Nature Cell Biology
Gao, Li and colleagues derive trophectoderm stem cells from 32-cell mouse embryos. These cells represent an early trophectoderm state and are capable of developing into placenta cells, forming placent...
www.nature.com
June 11, 2026 at 1:05 PM
Very nice work! Inhibition of Hippo signaling, activation of Wnt signaling and TGFbeta signaling give rise to MTSC. J Zhang: Mouse trophectoderm stem cells generated with morula signalling inducers capture an
early trophectoderm state
early trophectoderm state