Amelioration of radiation-induced fibrosis: inhibition of transforming growth factor-beta signaling by halofuginone. (Q40597763)

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17 November 2019

title

Amelioration of radiation-induced fibrosis: inhibition of transforming growth factor-beta signaling by halofuginone (English)

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17 November 2019

4

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17 November 2019

Alain Mauviel

5

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Anita B Roberts

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author name string

Sandhya Xavier

1

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17 November 2019

Ester Piek

2

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17 November 2019

Makiko Fujii

3

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Kathy C Flanders

6

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17 November 2019

Ayelet M Samuni

7

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17 November 2019

Angelina Felici

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17 November 2019

Michael Reiss

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17 November 2019

Shai Yarkoni

10

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17 November 2019

Anastasia Sowers

11

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James B Mitchell

12

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17 November 2019

Angelo Russo

14

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language of work or name

English

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publication date

19 January 2004

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Journal of Biological Chemistry

17 November 2019

published in

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17 November 2019

volume

279

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issue

15

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17 November 2019

page(s)

15167-15176

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The role of DNA double strand breaks in lonizing radiation-induced killing of eukaryotic cells

17 November 2019

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Mice lacking Smad3 are protected against cutaneous injury induced by ionizing radiation

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Halofuginone: an inhibitor of collagen type I synthesis

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Halofuginone, an inhibitor of type-I collagen synthesis and skin sclerosis, blocks transforming-growth-factor-beta-mediated Smad3 activation in fibroblasts.

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Halofuginone to prevent and treat thioacetamide-induced liver fibrosis in rats

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Use of vanadate as protein-phosphotyrosine phosphatase inhibitor

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Heterogeneity of hematopoietic cells immortalized by v-myc/v-raf recombinant retrovirus infection of bone marrow or fetal liver

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Functional characterization of transforming growth factor beta signaling in Smad2- and Smad3-deficient fibroblasts

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NEMO/IKK gamma-deficient mice model incontinentia pigmenti.

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Defective neural tube morphogenesis and altered apoptosis in the absence of both JNK1 and JNK2.

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Interference with transforming growth factor-beta/ Smad3 signaling results in accelerated healing of wounds in previously irradiated skin

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Smads 2 and 3 are differentially activated by transforming growth factor-beta (TGF-beta ) in quiescent and activated hepatic stellate cells. Constitutive nuclear localization of Smads in activated cells is TGF-beta-independent.

21 January 2018

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Targeted deletion of Smad4 shows it is required for transforming growth factor beta and activin signaling in colorectal cancer cells

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The Smad4 activation domain (SAD) is a proline-rich, p300-dependent transcriptional activation domain

21 January 2018

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Inhibition of transforming growth factor-beta/SMAD signalling by the interferon-gamma/STAT pathway.

21 January 2018

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Phosphatidylinositol 3-kinase function is required for transforming growth factor beta-mediated epithelial to mesenchymal transition and cell migration.

21 January 2018

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21 January 2018

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Identifiers

DOI

10.1074/JBC.M309798200

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:14732719%20AND%20SRC:MED&resulttype=core&format=json

17 November 2019

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