TGF-beta signaling by Smad proteins (Q22253317)

positive regulation of transcription, DNA-templated

GOA release 2020-03-11

1 reference

GOA release 2020-03-11

K Miyazono

1

K

Miyazono

1 reference

PubMed

PubMed publication ID

10708949

8 February 2023

publication date

2000

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Cytokine and Growth Factor Reviews

PubMed

language of work or name

English

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published in

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volume

11

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issue

1-2

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page(s)

15-22

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publication type of scholarly work

review article

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TGF-β signalling from cell membrane to nucleus through SMAD proteins

Europe PubMed Central

cites work

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TGF-beta signal transduction

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TGF-beta signaling by Smad proteins

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Bone morphogenetic protein-2 converts the differentiation pathway of C2C12 myoblasts into the osteoblast lineage

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Identification of a novel bone morphogenetic protein-responsive gene that may function as a noncoding RNA.

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Roles of bone morphogenetic protein type I receptors and Smad proteins in osteoblast and chondroblast differentiation.

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Signal transduction by bone morphogenetic proteins

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Specific Activation of Smad1 Signaling Pathways by the BMP7 Type I Receptor, ALK2

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Transforming growth factor beta1 induces nuclear export of inhibitory Smad7

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Chondrogenic differentiation of clonal mouse embryonic cell line ATDC5 in vitro: differentiation-dependent gene expression of parathyroid hormone (PTH)/PTH-related peptide receptor

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Human osteogenic protein-1 induces both chondroblastic and osteoblastic differentiation of osteoprogenitor cells derived from newborn rat calvaria

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p38 mitogen-activated protein kinase functionally contributes to chondrogenesis induced by growth/differentiation factor-5 in ATDC5 cells

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Transient gene transfer and expression of Smad7 prevents bleomycin-induced lung fibrosis in mice

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Human Smad3 and Smad4 Are Sequence-Specific Transcription Activators

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Direct binding of Smad3 and Smad4 to critical TGFbeta -inducible elements in the promoter of human plasminogen activator inhibitor-type 1gene

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Identification and functional characterization of a Smad binding element (SBE) in the JunB promoter that acts as a transforming growth factor-beta, activin, and bone morphogenetic protein-inducible enhancer

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Characterization of theMADH2/Smad2Gene, a HumanMadHomolog Responsible for the Transforming Growth Factor-β and Activin Signal Transduction Pathway

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Alternatively spliced variant of Smad2 lacking exon 3. Comparison with wild-type Smad2 and Smad3.

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A short amino-acid sequence in MH1 domain is responsible for functional differences between Smad2 and Smad3

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7 January 2021

Smad2 and Smad3 positively and negatively regulate TGF beta-dependent transcription through the forkhead DNA-binding protein FAST2

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Convergence of transforming growth factor-beta and vitamin D signaling pathways on SMAD transcriptional coactivators

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Targeted disruption of Cbfa1 results in a complete lack of bone formation owing to maturational arrest of osteoblasts

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Cbfa1, a candidate gene for cleidocranial dysplasia syndrome, is essential for osteoblast differentiation and bone development

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AML1, the target of multiple chromosomal translocations in human leukemia, is essential for normal fetal liver hematopoiesis

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Interaction and functional cooperation of PEBP2/CBF with Smads. Synergistic induction of the immunoglobulin germline Calpha promoter

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Smad and AML proteins synergistically confer transforming growth factor beta1 responsiveness to human germ-line IgA genes

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Role of p300, a transcriptional coactivator, in signalling of TGF-beta

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The tumor suppressor Smad4/DPC4 and transcriptional adaptor CBP/p300 are coactivators for Smad3 in TGF-β-induced transcriptional activation

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TGF-β-stimulated cooperation of Smad proteins with the coactivators CBP/p300

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Physical and functional interaction of SMADs and p300/CBP

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TGF-beta-induced phosphorylation of Smad3 regulates its interaction with coactivator p300/CREB-binding protein

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E1A inhibits transforming growth factor-beta signaling through binding to Smad proteins

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Synergistic signaling in fetal brain by STAT3-Smad1 complex bridged by p300

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A Smad transcriptional corepressor

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Ski is a component of the histone deacetylase complex required for transcriptional repression by Mad and thyroid hormone receptor

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c-Ski acts as a transcriptional co-repressor in transforming growth factor-beta signaling through interaction with smads

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The Ski oncoprotein interacts with the Smad proteins to repress TGFbeta signaling

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Interaction of the Ski oncoprotein with Smad3 regulates TGF-beta signaling

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Negative feedback regulation of TGF-beta signaling by the SnoN oncoprotein

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10.1016/S1359-6101(99)00025-8

Identifiers

DOI

1 reference

Consolidated OpenCitations Corpus – April 2017

1 reference

Consolidated OpenCitations Corpus – April 2017

PubMed publication ID

10708949

1 reference

Consolidated OpenCitations Corpus – April 2017