dephosphorylation


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de•phos•pho•ryl•a•tion

(diˈfɒs fər əˈleɪ ʃən)

n.
1. the removal of a phosphate group from an organic compound.
2. the resulting state or condition.
[1930–35; de- + phosphoryl the radical PO + -ation]
Random House Kernerman Webster's College Dictionary, © 2010 K Dictionaries Ltd. Copyright 2005, 1997, 1991 by Random House, Inc. All rights reserved.
References in periodicals archive ?
ChREBP is translocated to the nucleus and binds to DNA after dephosphorylation of a p-Ser and a p-Thr residue by PP2A, which itself is activated by Xylulose-5-phosphate (Xu5p).
reported that CA intensifies the dephosphorylation of phytate in vitro.
Although auto dephosphorylation of response regulator has been reported (45), in many cases it occurs through catalysis by another protein.
In fact, Lnc-DC binds directly with the C terminus of STAT3, thus promoting STAT3 phosphorylation on tyrosine-705 by preventing STAT3 dephosphorylation. Preeclampsia patients were found to have enhanced Lnc-DC expression and STAT3 phosphorylation in the deciduas, along with increased proportion of decidual mature DCs and a bias of [CD4.sup.+] T cell differentiation into Th1 phenotype [36].
YAP dephosphorylation leads to its inactivation, followed by cytoplasmic retention when the Hippo pathway is "switched on." However, when the pathway is "switched off," YAP is phosphorylated and accumulates in the nucleus, promoting cellular proliferation, metastasis, or regeneration [3, 4].
There are several ways to generate ceramide in mammalian cells (Figure 1): hydrolysis of sphingomyelin, de novo synthesis from palmitoyl-CoA and serine, catabolism of glucosylceramide and galactosylceramide, synthesis from sphingosine and fatty acid, and dephosphorylation of ceramide-1-phosphate.
This formation can be reversed by tumor suppressor PTEN that catalyzes PIP3 dephosphorylation into PIP2.
The cellulase gene expression can also be regulated by the dynamics of protein phosphorylation and dephosphorylation involving protein kinases and phosphatases [34], respectively.
RhoA effectors, ROCK I/II, regulate the actomyosin complex by inhibiting MLC dephosphorylation. Phosphorylation by ROCK inactivates a myosin phosphatase, retaining myosin II in the phosphorylated or active state [34, 35].
In androgen-dependent but also in androgen-independent prostate cancer cell lines, melatonin (1 mM) seemed to exert an antiangiogenic effect since it reduced hypoxia-inducible factor (HIF-1) protein levels and the release of the vascular endothelial growth factor, which correlated with dephosphorylation of p70S6 kinase and its target, ribosomal protein RPS6 [85].
While LTP has been historically ascribed to kinase activity and LTD to dephosphorylation and phosphatase activity [3], a common effector system capable of decoding [Ca.sup.2+] spike frequency into different functional outputs would be strategically positioned to regulate both LTP and LTD.