The murine type II TGF-beta receptor has a coincident embryonic expression and binding preference for TGF-beta 1

Development ◽  
1994 ◽  
Vol 120 (1) ◽  
pp. 165-175 ◽  
Author(s):  
S. Lawler ◽  
A.F. Candia ◽  
R. Ebner ◽  
L. Shum ◽  
A.R. Lopez ◽  
...  
Keyword(s):  
Receptor Expression ◽  
Type Ii ◽  
Tgf Beta ◽  
Mouse Fetus ◽  
Beta Receptor ◽  
Receptor Isoforms ◽  
Binding Preference ◽  
Preferential Binding ◽  
The Central Nervous System ◽  
Beta 2

We have isolated cDNAs of the murine type II TGF-beta receptor and have found a conserved cytoplasmic domain, but a less extensive homology in the extracellular receptor domain between the human and murine homologues. In situ hybridization analysis of the mouse fetus during mid gestation localized the expression of this receptor to various developing tissues, primarily in the mesenchyme and epidermis. This expression pattern correlates well with the expression of TGF-beta in general and especially TGF-beta 1, suggesting that TGF-beta 1 exerts its developmental role through this receptor in an autocrine or paracrine fashion. Type II receptor expression was not detected in the central nervous system and developing cartilage. These tissues lack TGF-beta 1 expression but express TGF-beta 2 and/or TGF-beta 3, suggesting that they may exert their activities through separate receptor isoforms. In addition, the efficient binding of TGF-beta 1, but not TGF-beta 2, to the cloned type II receptor strengthens the likelihood that additional type II receptor isoforms exist which display preferential binding to TGF-beta 2 and have their own defined role in development.

scholarly journals Plasmin cleaves betaglycan and releases a 60 kDa transforming growth factor-β complex from the cell surface

1994 ◽  
Vol 302 (1) ◽  
pp. 199-205 ◽  
Author(s):  
J Lamarre ◽  
J Vasudevan ◽  
S L Gonias
Keyword(s):  
Growth Factor ◽  
Cell Surface ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Type I ◽  
Type Ii ◽  
Tgf Beta ◽  
Beta Receptor ◽  
Cell Extracts ◽  
Beta 2

Plasmin regulates the activity and distribution of transforming growth factor beta (TGF-beta) and other growth factors. The purpose of the present investigation was to determine the effects of plasmin on cellular receptors for TGF-beta. AKR-2B fibroblasts were affinity-labelled with 125I-TGF-beta 1 and 125I-TGF-beta 2, demonstrating betaglycan, the type-I TGF-beta receptor and the type-II TGF-beta receptor. Treatment of TGF-beta-affinity-labelled cells with plasmin (10-100 nM) for 1 h profoundly and selectively decreased recovery of TGF-beta-betaglycan complex. The type-I and type-II receptors were not plasmin substrates. A radiolabelled complex with an apparent mass of 60 kDa was detected by SDS/PAGE in both the medium and cell extracts of plasmin-treated affinity-labelled cells. In order to demonstrate that plasmin cleavage of betaglycan did not require prior exposure of the betaglycan to cross-linking agent, AKR-2B cells were treated with plasmin first and then affinity-labelled. Markedly decreased TGF-beta binding to cellular betaglycan was observed. Although plasmin treatment of AKR-2B cells decreased overall binding of 125I-TGF-beta 1 and 125I-TGF-beta 2, the rate at which the cells degraded bound 125I-TGF-beta at 37 degrees C was not changed. AKR-2B cells treated with plasmin demonstrated slightly increased [3H]thymidine incorporation; the plasmin-treated cells retained their ability to respond to TGF-beta. Conditioned medium from plasmin-treated AKR-2B cells contained increased amounts of active TGF-beta as determined in Mv 1 Lu epithelial-cell-proliferation assays. Specific cleavage of betaglycan represents a novel mechanism whereby plasmin may regulate the assortment of receptors available for TGF-beta. In addition, plasmin may facilitate transfer of active TGF-beta between neighbouring cells by releasing the active growth factor from the cell surface.

scholarly journals Control of TGF-beta receptor expression in bone

10.2741/a268 ◽  
1998 ◽  
Vol 3 (4) ◽  
pp. d113-124 ◽  
Author(s):  
Michael Centrella
Keyword(s):  
Receptor Expression ◽  
Tgf Beta ◽  
Beta Receptor

TGF-beta stimulates rat mesangial cell proliferation in culture: role of PDGF beta-receptor expression

1993 ◽  
Vol 264 (2) ◽  
pp. F199-F205 ◽  
Author(s):  
U. Haberstroh ◽  
G. Zahner ◽  
M. Disser ◽  
F. Thaiss ◽  
G. Wolf ◽  
...  
Keyword(s):  
Growth Factor ◽  
Dna Synthesis ◽  
Transforming Growth Factor ◽  
Mesangial Cell ◽  
Kinetic Studies ◽  
Receptor Expression ◽  
Tgf Beta ◽  
Beta Receptor ◽  
Cell Counts

Transforming growth factor (TGF)-beta is known to increase mesangial cell (MC) matrix; however, its possible role on MC proliferation is controversial. We therefore studied the influence of TGF-beta on MC proliferation in culture and evaluated its effect on the platelet-derived growth factor (PDGF) B-chain as well as the expression of the PDGF beta-receptor. TGF-beta (1 ng/ml) increases MC DNA synthesis by approximately threefold after 48 h of incubation. TGF-beta-induced MC proliferation was also confirmed by cell counts. A neutralizing anti-TGF-beta antibody completely blocked this growth promoting activity. The levels of PDGF beta-receptor steady-state mRNA were increased by TGF-beta at 48 h. This was associated with an increase in receptor density per cell as measured by receptor kinetic studies. PDGF B-chain mRNA was also increased by TGF-beta at 48 h. A neutralizing anti-PDGF B-antibody causes no reduction of TGF-beta-induced DNA synthesis; however, suramin completely inhibited the mitogenic effect of TGF-beta. We conclude that TGF-beta stimulates MC growth in long-term culture, a process in which upregulation of the PDGF beta-receptor and enhanced synthesis of PDGF B-chain might be involved.

Cloning of a type I TGF-beta receptor and its effect on TGF-beta binding to the type II receptor

Science ◽  
1993 ◽  
Vol 260 (5112) ◽  
pp. 1344-1348 ◽  
Author(s):  
R Ebner ◽  
R. Chen ◽  
L Shum ◽  
S Lawler ◽  
T. Zioncheck ◽  
...  
Keyword(s):  
Type I ◽  
Type Ii ◽  
Tgf Beta ◽  
Beta Receptor

Inactivation of the type II TGF-beta receptor in colon cancer cells with microsatellite instability

Science ◽  
1995 ◽  
Vol 268 (5215) ◽  
pp. 1336-1338 ◽  
Author(s):  
S Markowitz ◽  
J Wang ◽  
L Myeroff ◽  
R Parsons ◽  
L Sun ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Microsatellite Instability ◽  
Cancer Cells ◽  
Type Ii ◽  
Colon Cancer Cells ◽  
Tgf Beta ◽  
Beta Receptor

Truncated type II TGF-beta receptor promotes liver regeneration in dimetylnitrosamin-treated cirrohotic rats

2002 ◽  
Vol 36 ◽  
pp. 28
Author(s):  
Toru Nakamura ◽  
Ryuichiro Sakata ◽  
Masaharu Sakamoto ◽  
Takuji Torimura ◽  
Takato Ueno ◽  
...  
Keyword(s):  
Liver Regeneration ◽  
Type Ii ◽  
Tgf Beta ◽  
Beta Receptor

scholarly journals Abnormal expression of TGF-beta type II receptor isoforms contributes to acute myeloid leukemia

Oncotarget ◽  
2016 ◽  
Vol 8 (6) ◽  
pp. 10037-10049 ◽  
Author(s):  
Yong Wu ◽  
Min Su ◽  
ShuX Zhang ◽  
Yu Cheng ◽  
Xiao Y. Liao ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Type Ii ◽  
Tgf Beta ◽  
Abnormal Expression ◽  
Receptor Isoforms ◽  
Acute Myeloid
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