Thr709
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Home > Phosphorylation Site Page: > Thr709  -  Fe65 (human)

Site Information
PKRLGAHtP______   SwissProt Entrez-Gene
Blast this site against: NCBI  SwissProt  PDB 
Site Group ID: 451149

In vivo Characterization
Methods used to characterize site in vivo:
electrophoretic mobility shift ( 4 ) , mass spectrometry ( 1 , 2 , 3 , 4 ) , mutation of modification site ( 4 )
Disease tissue studied:
breast cancer ( 3 ) , breast ductal carcinoma ( 3 ) , HER2 positive breast cancer ( 2 ) , luminal A breast cancer ( 2 ) , luminal B breast cancer ( 2 ) , breast cancer, surrounding tissue ( 2 ) , breast cancer, triple negative ( 2 , 3 ) , neuroblastoma ( 1 )
Relevant cell line - cell type - tissue:

Upstream Regulation
Putative in vivo kinases:
ERK2 (human) ( 4 )
Kinases, in vitro:
ERK2 (human) ( 4 )
Treatments:
ischemia ( 3 ) , phorbol_ester ( 4 ) , U0126 ( 4 )

References 

1

Borenäs M, et al. (2024) ALK signaling primes the DNA damage response sensitizing ALK-driven neuroblastoma to therapeutic ATR inhibition. Proc Natl Acad Sci U S A 121, e2315242121
38154064   Curated Info

2

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

3

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

4

Standen CL, et al. (2003) The neuronal adaptor protein Fe65 is phosphorylated by mitogen-activated protein kinase (ERK1/2). Mol Cell Neurosci 24, 851-7
14697653   Curated Info