Ser123
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Home > Phosphorylation Site Page: > Ser123  -  IGFBP1 (human)

Site Information
AEAGsPEsPEstEIT   SwissProt Entrez-Gene
Blast this site against: NCBI  SwissProt  PDB 
Site Group ID: 4668105

In vivo Characterization
Methods used to characterize site in vivo:
2D analysis ( 5 ) , electrophoretic mobility shift ( 10 ) , immunoprecipitation ( 1 , 7 ) , mass spectrometry ( 1 , 3 , 4 , 6 , 7 , 8 , 9 , 10 ) , multiple reaction monitoring (MRM) ( 2 ) , mutation of modification site ( 5 ) , phospho-antibody ( 3 , 4 , 5 ) , western blotting ( 3 , 4 , 5 )
Disease tissue studied:
endometrial cancer ( 2 ) , liver cancer ( 1 , 4 , 10 ) , Fetal growth restriction ( 6 , 9 )
Relevant cell line - cell type - tissue:
amniotic fluid ( 6 , 7 , 8 , 9 ) , CHO (fibroblast) ( 5 ) , endometrial stromal ( 2 ) , HepG2 (hepatic) ( 1 , 4 , 10 ) , stromal ( 3 )

Upstream Regulation
Putative in vivo kinases:
PKCA (human) ( 1 )
Treatments:
amino_acid_starvation ( 10 ) , bisindolylmaleimide_II ( 1 ) , hypoxia ( 2 , 10 ) , leucine_deprivation ( 3 ) , phorbol_ester ( 1 ) , rapamycin ( 2 ) , siRNA ( 1 ) , TBB ( 1 )

Downstream Regulation
Effects of modification on IGFBP1:
activity, inhibited ( 2 ) , molecular association, regulation ( 2 , 6 )
Effects of modification on biological processes:
signaling pathway regulation ( 2 )
Induce interaction with:
CK2B (human) ( 2 ) , IGF1 (human) ( 6 )

Disease / Diagnostics Relevance
Relevant diseases:
Fetal growth restriction ( 6 )

References 

1

Chen AW, et al. (2021) IGFBP-1 hyperphosphorylation in response to nutrient deprivation is mediated by activation of protein kinase Cα (PKCα). Mol Cell Endocrinol 536, 111400
34314739   Curated Info

2

Abu Shehab M, et al. (2020) Inhibition of decidual IGF-1 signaling in response to hypoxia and leucine deprivation is mediated by mTOR and AAR pathways and increased IGFBP-1 phosphorylation. Mol Cell Endocrinol 512, 110865
32502935   Curated Info

3

Shehab MA, et al. (2017) Exposure of decidualized HIESC to low oxygen tension and leucine deprivation results in increased IGFBP-1 phosphorylation and reduced IGF-I bioactivity. Mol Cell Endocrinol 452, 1-14
28435049   Curated Info

4

Damerill I, et al. (2016) Hypoxia Increases IGFBP-1 Phosphorylation Mediated by mTOR Inhibition. Mol Endocrinol 30, 201-16
26714229   Curated Info

5

Abu Shehab M, et al. (2013) Phosphorylation of IGFBP-1 at Discrete Sites Elicits Variable Effects on IGF-I Receptor Autophosphorylation. Endocrinology 154, 1130-43
23354097   Curated Info

6

Abu Shehab M, et al. (2010) Site-specific IGFBP-1 hyper-phosphorylation in fetal growth restriction: clinical and functional relevance. J Proteome Res 9, 1873-81
20143870   Curated Info

7

Abu Shehab M, Inoue S, Han VK, Gupta MB (2009) Site specific phosphorylation of insulin-like growth factor binding protein-1 (IGFBP-1) for evaluating clinical relevancy in fetal growth restriction. J Proteome Res 8, 5325-35
19731965   Curated Info

8

Dolcini L, et al. (2009) Identification of the amniotic fluid insulin-like growth factor binding protein-1 phosphorylation sites and propensity to proteolysis of the isoforms. FEBS J 276, 6033-46
19765076   Curated Info

9

Nissum M, et al. (2009) Functional and complementary phosphorylation state attributes of human insulin-like growth factor-binding protein-1 (IGFBP-1) isoforms resolved by free flow electrophoresis. Mol Cell Proteomics 8, 1424-35
19193607   Curated Info

10

Seferovic MD, et al. (2009) Hypoxia and leucine deprivation induce human insulin-like growth factor binding protein-1 hyperphosphorylation and increase its biological activity. Endocrinology 150, 220-31
18772238   Curated Info