PMID- 2170414
OWN - NLM
STAT- MEDLINE
DCOM- 19901115
LR  - 20220331
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 265
IP  - 30
DP  - 1990 Oct 25
TI  - Concomitant loss of transforming growth factor (TGF)-beta receptor types I and II 
      in TGF-beta-resistant cell mutants implicates both receptor types in signal 
      transduction.
PG  - 18518-24
AB  - A panel of 71 chemically mutagenized Mv1Lu mink lung epithelial cell clones were 
      selected based on their resistance to the growth inhibitory action of 
      transforming growth factor beta 1 (TGF-beta 1) and TGF-beta 2. Characterization 
      of TGF-beta receptors in these mutants indicates that the TGF-beta-binding 
      membrane proteoglycan, betaglycan, is apparently normal in all of them. However, 
      14 of the mutant clones are defective in TGF-beta receptor type I, and 22 clones 
      are simultaneously defective in receptor types I and II. The clones with type I 
      receptor defects fall into two distinct phenotypes, called R and LR. The R 
      phenotype is characterized by the lack of detectable type I receptors, and has 
      been previously described (Boyd, F. T., and Massague, J. (1989) J. Biol. Chem. 
      264, 2272-2278). LR mutants are characterized by expression of low levels of type 
      I receptor and are, like the R mutants, completely resistant to growth inhibition 
      by TGF-beta 1 or -beta 2. Mutant clones that are simultaneously defective in 
      receptor types I and II fall into three distinct phenotypes. These included DRa 
      mutants which are characterized by lack of detectable receptor types I and II, 
      DRb mutants which are characterized by low expression of both receptor types and 
      an anomalously fast electrophoretic mobility of the type II receptor protein. All 
      mutants that have a low level of type II receptor are also defective in type I 
      receptor. In addition to the loss of growth inhibitory response, the 
      receptor-defective mutants described here have lost all other responses to 
      TGF-beta 1 and -beta 2 known to occur in parental Mv1Lu cells. The defects 
      present in these mutant clones are not encountered in clones isolated from 
      nonmutagenized parental Mv1Lu cells or in mutagenized cells that had not been 
      exposed to selection with TGF-beta. The results implicate TGF-beta receptor types 
      I and II in the mediation of a common set of cellular responses to TGF-beta. 
      Furthermore, the high relative frequency of isolation of DR mutants raises the 
      possibility that receptor types I and II interact as part of a common signaling 
      TGF-beta receptor complex.
FAU - Laiho, M
AU  - Laiho M
AD  - Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, New 
      York, New York 10021.
FAU - Weis, M B
AU  - Weis MB
FAU - Massague, J
AU  - Massague J
LA  - eng
GR  - CA-34610/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Affinity Labels)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Receptors, Transforming Growth Factor beta)
RN  - 0 (Transforming Growth Factor beta)
SB  - IM
MH  - Affinity Labels
MH  - Animals
MH  - Cell Line
MH  - Clone Cells
MH  - Mink
MH  - Mutation
MH  - Receptors, Cell Surface/classification/genetics/*physiology
MH  - Receptors, Transforming Growth Factor beta
MH  - Signal Transduction
MH  - Transforming Growth Factor beta/*physiology
EDAT- 1990/10/25 00:00
MHDA- 1990/10/25 00:01
CRDT- 1990/10/25 00:00
PHST- 1990/10/25 00:00 [pubmed]
PHST- 1990/10/25 00:01 [medline]
PHST- 1990/10/25 00:00 [entrez]
AID - S0021-9258(17)44782-X [pii]
PST - ppublish
SO  - J Biol Chem. 1990 Oct 25;265(30):18518-24.