Thr8
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Home > Phosphorylation Site Page: > Thr8  -  SMAD3 (human)

Site Information
MSSILPFtPPIVkRL   SwissProt Entrez-Gene
Blast this site against: NCBI  SwissProt  PDB 
Site Group ID: 452179

In vivo Characterization
Methods used to characterize site in vivo:
[32P] bio-synthetic labeling ( 16 ) , mass spectrometry ( 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 13 , 14 ) , mutation of modification site ( 12 , 16 ) , phospho-antibody ( 11 , 15 , 16 ) , western blotting ( 11 , 15 )
Disease tissue studied:
breast cancer ( 4 , 12 , 15 ) , breast ductal carcinoma ( 4 ) , HER2 positive breast cancer ( 1 ) , luminal A breast cancer ( 1 ) , luminal B breast cancer ( 1 ) , breast cancer, triple negative ( 1 , 4 ) , cervical cancer ( 13 ) , cervical adenocarcinoma ( 13 ) , lung cancer ( 9 ) , non-small cell lung cancer ( 9 ) , melanoma skin cancer ( 2 , 11 )
Relevant cell line - cell type - tissue:

Upstream Regulation
Putative in vivo kinases:
CDK2 (mouse) ( 16 ) , CDK4 (mouse) ( 12 , 16 )
Treatments:
SB203580 ( 15 ) , TGF-beta ( 15 ) , Y27632 ( 15 )

Downstream Regulation
Effects of modification on biological processes:
cell cycle regulation ( 12 , 16 ) , transcription, altered ( 16 ) , transcription, inhibited ( 12 )

References 

1

Mertins P, et al. (2016) Proteogenomics connects somatic mutations to signalling in breast cancer. Nature 534, 55-62
27251275   Curated Info

2

Stuart SA, et al. (2015) A Phosphoproteomic Comparison of B-RAFV600E and MKK1/2 Inhibitors in Melanoma Cells. Mol Cell Proteomics 14, 1599-615
25850435   Curated Info

3

Sharma K, et al. (2014) Ultradeep human phosphoproteome reveals a distinct regulatory nature of Tyr and Ser/Thr-based signaling. Cell Rep 8, 1583-94
25159151   Curated Info

4

Mertins P, et al. (2014) Ischemia in tumors induces early and sustained phosphorylation changes in stress kinase pathways but does not affect global protein levels. Mol Cell Proteomics 13, 1690-704
24719451   Curated Info

5

Luerman GC, et al. (2014) Phosphoproteomic evaluation of pharmacological inhibition of leucine-rich repeat kinase 2 reveals significant off-target effects of LRRK-2-IN-1. J Neurochem 128, 561-76
24117733   Curated Info

6

Kim JY, et al. (2013) Dissection of TBK1 signaling via phosphoproteomics in lung cancer cells. Proc Natl Acad Sci U S A 110, 12414-9
23836654   Curated Info

7

Mertins P, et al. (2013) Integrated proteomic analysis of post-translational modifications by serial enrichment. Nat Methods 10, 634-7
23749302   Curated Info

8

Zhou H, et al. (2013) Toward a comprehensive characterization of a human cancer cell phosphoproteome. J Proteome Res 12, 260-71
23186163   Curated Info

9

Klammer M, et al. (2012) Phosphosignature predicts dasatinib response in non-small cell lung cancer. Mol Cell Proteomics 11, 651-68
22617229   Curated Info

10

Beli P, et al. (2012) Proteomic Investigations Reveal a Role for RNA Processing Factor THRAP3 in the DNA Damage Response. Mol Cell 46, 212-25
22424773   Curated Info

11

Cohen-Solal KA, et al. (2011) Constitutive Smad linker phosphorylation in melanoma: a mechanism of resistance to transforming growth factor-β-mediated growth inhibition. Pigment Cell Melanoma Res 24, 512-24
21477078   Curated Info

12

Zelivianski S, Cooley A, Kall R, Jeruss JS (2010) Cyclin-dependent kinase 4-mediated phosphorylation inhibits smad3 activity in cyclin d-overexpressing breast cancer cells. Mol Cancer Res 8, 1375-87
20736297   Curated Info

13

Olsen JV, et al. (2010) Quantitative phosphoproteomics reveals widespread full phosphorylation site occupancy during mitosis. Sci Signal 3, ra3
20068231   Curated Info

14

Gauci S, et al. (2009) Lys-N and trypsin cover complementary parts of the phosphoproteome in a refined SCX-based approach. Anal Chem 81, 4493-501
19413330   Curated Info

15

Kamaraju AK, Roberts AB (2005) Role of Rho/ROCK and p38 MAP kinase pathways in transforming growth factor-beta-mediated Smad-dependent growth inhibition of human breast carcinoma cells in vivo. J Biol Chem 280, 1024-36
15520018   Curated Info

16

Matsuura I, et al. (2004) Cyclin-dependent kinases regulate the antiproliferative function of Smads. Nature 430, 226-31
15241418   Curated Info

17

Liu X, et al. (1997) Transforming growth factor beta-induced phosphorylation of Smad3 is required for growth inhibition and transcriptional induction in epithelial cells. Proc Natl Acad Sci U S A 94, 10669-74
9380693   Curated Info