N
Nils-Erik Heldin
Researcher at Uppsala University
Publications - 47
Citations - 4439
Nils-Erik Heldin is an academic researcher from Uppsala University. The author has contributed to research in topics: Cell culture & Thyrotropin receptor. The author has an hindex of 27, co-authored 47 publications receiving 4306 citations. Previous affiliations of Nils-Erik Heldin include Uppsala University Hospital.
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Journal ArticleDOI
Identification of Smad7, a TGFβ-inducible antagonist of TGF-β signalling
Atsuhito Nakao,Mozhgan Afrakhte,Anita Morn,Takuya Nakayama,Jan L. Christian,Rainer Heuchel,Susumu Itoh,Masahiro Kawabata,Nils-Erik Heldin,Carl-Henrik Heldin,Peter ten Dijke +10 more
TL;DR: In this paper, the authors reported the identification of Smad7, which is related to Smad6 (ref. 13) and showed that TGF-β-mediated phosphorylation of two proteins, Smad2 and Smad3, is inhibited by Smad-7, indicating that the antagonistic effect of the protein is exerted at this important regulatory step.
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Induction of inhibitory smad6 and smad7 mrna by tgf-beta family members
Mozhgan Afrakhte,Anita Morén,Surinder Jossan,Susumu Itoh,Kuber T. Sampath,Bengt Westermark,Carl-Henrik Heldin,Nils-Erik Heldin,Peter ten Dijke +8 more
TL;DR: The isolation of human Smad6 is reported, which is closely related to Smad7, to show that expression of inhibitory Smads is induced by multiple stimuli, including the various TGF-beta family members, whose action they antagonize.
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Transforming Growth Factor β1 Induces Nuclear Export of Inhibitory Smad7
Susumu Itoh,Maréne Landström,Annika Hermansson,Fumiko Itoh,Carl-Henrik Heldin,Nils-Erik Heldin,Peter ten Dijke +6 more
TL;DR: It is reported that Smad7, but not Smad6, inhibits TGF-β1-induced growth inhibition and the expression of immediate early response genes, including Smad 7, which suggests a functional role distinct from its antagonistic effect in receptor-mediated Smad activation.
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Transforming growth factor-beta and epidermal growth factor synergistically stimulate epithelial to mesenchymal transition (EMT) through a MEK-dependent mechanism in primary cultured pig thyrocytes.
TL;DR: The observations indicate that concomitant growth factor-induced MEK activation is necessary for TGF-β1 to convert normal thyroid epithelial cells to a mesenchymal phenotype.
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Transforming Growth Factor-β1 (TGF-β)–induced Apoptosis of Prostate Cancer Cells Involves Smad7-dependent Activation of p38 by TGF-β-activated Kinase 1 and Mitogen-activated Protein Kinase Kinase 3
Sofia Edlund,Shizhong Bu,Norbert Schuster,Pontus Aspenström,Rainer Heuchel,Nils-Erik Heldin,Peter ten Dijke,Carl-Henrik Heldin,Maréne Landström +8 more
TL;DR: The inhibitory Smad7, a direct target gene for transforming growth factor-β (TGF-β), mediates TGF- β1–induced apoptosis in several cell types and reports that apoptosis of human prostate cancer patients is reported.