scholarly journals Loss of Transforming Growth Factor-β (TGF-β) Receptor Type I Mediates TGF-β Resistance in Human Papillomavirus Type 16-Transformed Human Keratinocytes at Late Stages of in Vitro Progression

Virology ◽  
2000 ◽  
Vol 270 (2) ◽  
pp. 408-416 ◽  
Author(s):  
Yi-de Mi ◽  
Darrell R. Borger ◽  
Pearl R. Fernandes ◽  
Lucia Pirisi ◽  
Kim E. Creek
Keyword(s):  
Human Papillomavirus ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Human Keratinocytes ◽  
Transforming Growth Factor Β ◽  
Type I ◽  
Human Papillomavirus Type 16 ◽  
Β Receptor ◽  
Late Stages

scholarly journals A Novel Protein Distinguishes between Quiescent and Activated Forms of the Type I Transforming Growth Factor β Receptor

1998 ◽  
Vol 273 (16) ◽  
pp. 9365-9368 ◽  
Author(s):  
Min-Ji Charng ◽  
Dou Zhang ◽  
Paı̈vi Kinnunen ◽  
Michael D. Schneider
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Type I ◽  
Β Receptor ◽  
Novel Protein

Adenovirus-Mediated Transmission of a Dominant Negative Transforming Growth Factor-β Receptor Inhibits In Vitro Mouse Cranial Suture Fusion

2002 ◽  
Vol 110 (2) ◽  
pp. 506-514 ◽  
Author(s):  
Babak J. Mehrara ◽  
Jason A. Spector ◽  
Joshua A. Greenwald ◽  
Hikari Ueno ◽  
Michael T. Longaker
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Dominant Negative ◽  
Cranial Suture ◽  
Suture Fusion ◽  
Β Receptor

scholarly journals Transforming Growth Factor-β Receptor Type I-dependent Fibrogenic Gene Program Is Mediated via Activation of Smad1 and ERK1/2 Pathways

2007 ◽  
Vol 282 (14) ◽  
pp. 10405-10413 ◽  
Author(s):  
Jaspreet Pannu ◽  
Sashidhar Nakerakanti ◽  
Edwin Smith ◽  
Peter ten Dijke ◽  
Maria Trojanowska
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Receptor Type ◽  
Type I ◽  
Β Receptor

Abstract 17285: A Selective Transforming Growth Factor-β and Growth Differentiation Factor-15 Ligand Trap Attenuates Pulmonary Hypertension

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Lai-Ming Yung ◽  
Samuel D Paskin-Flerlage ◽  
Ivana Nikolic ◽  
Scott Pearsall ◽  
Ravindra Kumar ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Type I ◽  
Rna Seq ◽  
Differentiation Factor ◽  
Group I ◽  
Tgf Β1

Introduction: Excessive Transforming Growth Factor-β (TGF-β) signaling has been implicated in pulmonary arterial hypertension (PAH), based on activation of TGF-β effectors and transcriptional targets in affected lungs and the ability of TGF-β type I receptor (ALK5) inhibitors to improve experimental PAH. However, clinical use of ALK5 inhibitors has been limited by cardiovascular toxicity. Hypothesis: We tested whether or not selective blockade of TGF-β and Growth Differentiation Factor (GDF) ligands using a recombinant TGFβ type II receptor extracellular domain Fc fusion protein (TGFBRII-Fc) could impact experimental PAH. Methods: Male SD rats were injected with monocrotaline (MCT) and received vehicle or TGFBRII-Fc (15 mg/kg, twice per week, i.p.). C57BL/6 mice were treated with SU-5416 and hypoxia (SUGEN-HX) and received vehicle or TGFBRII-Fc. RNA-Seq was used to profile transcriptional changes in lungs of MCT rats. Circulating levels of GDF-15 were measured in 241 PAH patients and 41 healthy controls. Human pulmonary artery smooth muscle cells were used to examine signaling in vitro . Results: TGFBRII-Fc is a selective ligand trap, inhibiting the ability of GDF-15, TGF-β1, TGF-β3, but not TGF-β2 to activate SMAD2/3 in vitro . In MCT rats, prophylactic treatment with TGFBRII-Fc normalized expression of TGF-β transcriptional target PAI-1, attenuated PAH and vascular remodeling. Delayed administration of TGFBRII-Fc in rats with established PAH at 2.5 weeks led to improved survival, decreased PAH and remodeling at 5 weeks. Similar findings were observed in SUGEN-HX mice. No valvular abnormalities were found with TGFBRII-Fc treatment. RNA-Seq revealed GDF-15 to be the most highly upregulated TGF-β ligand in the lungs of MCT rats, with only modest increases in TGF-β1 and no change in TGF-β2/3 observed, suggesting a dominant role of GDF-15 in the pathophysiology of this model. Plasma levels of GDF-15 were significantly increased in patients with diverse etiologies of WHO Group I PAH. Conclusions: These findings demonstrate that a selective TGF-β/GDF-15 trap attenuates experimental PAH, remodeling and mortality, without causing valvulopathy. These data highlight the potential role of GDF-15 as a pathogenic molecule and therapeutic target in PAH.

scholarly journals Repression of transforming growth factor-β receptor type I promoter expression by Sp1 deficiency

Oncogene ◽  
2000 ◽  
Vol 19 (40) ◽  
pp. 4660-4667 ◽  
Author(s):  
Sumudra Periyasamy ◽  
Sudhakar Ammanamanchi ◽  
Manoranjani PM Tillekeratne ◽  
Michael G Brattain
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Receptor Type ◽  
Type I ◽  
Β Receptor
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