Protein kinase D directly phosphorylates histone deacetylase 5 via a random sequential kinetic mechanism

Huynh, Quang Khai; McKinsey, Timothy A.

doi:10.1016/j.abb.2006.02.014

Cited by 57 publications

(51 citation statements)

References 39 publications

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“…Some class IIa HDAC kinases may display preferences toward specific 14-3-3 sites. In vitro, PKD is much less effective at phosphorylating Ser 259 than Ser 498 of HDAC5 (Huynh and McKinsey, 2006). In contrast, MARK2 and -3 were shown to uniquely phosphorylate Ser 155 but not other 14-3-3 sites of HDAC7 (Dequiedt et al, 2006).…”

Section: Subcellular Distributionmentioning

confidence: 92%

Class IIa histone deacetylases: regulating the regulators

2007

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Section: Subcellular Distributionmentioning

confidence: 92%

Class IIa histone deacetylases: regulating the regulators

2007

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“…Phosphorylation-dependant nuclear export of HDAC4 and HDAC5 results in de-repression of downstream target genes. 25,28 Reduction of the PRKD1 kinase activity could explain the de-repression of FOXG1 transcription in patients 3, 5, and 7 whereas an increased kinase activity could downregulate FOXG1 expression in patient 8. To date, no clinical Although unlikely, mutations in PRKD1 could be responsible for a clinical condition overlapping the FOXG1/congenital RTT.…”

Section: Discussionmentioning

confidence: 99%

“…Protein kinase D1 stimulates DNA synthesis and cell proliferation, and phosphorylates histone deacetylase (HDAC) 5 that is involved in control of chromatin structure and gene expression. 25,26 Protein kinase D1 also controls dendritic arborisation in hippocampal neurons. 27 The PRKD1 kinase phosphorylates class II HDACs.…”

Section: Discussionmentioning

confidence: 99%

14q12 and severe Rett-like phenotypes: new clinical insights and physical mapping of FOXG1-regulatory elements

et al. 2012

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The Forkhead box G1 (FOXG1) gene has been implicated in severe Rett-like phenotypes. It encodes the Forkhead box protein G1, a winged-helix transcriptional repressor critical for forebrain development. Recently, the core FOXG1 syndrome was defined as postnatal microcephaly, severe mental retardation, absent language, dyskinesia, and dysgenesis of the corpus callosum. We present seven additional patients with a severe Rett-like neurodevelopment disorder associated with de novo FOXG1 point mutations (two cases) or 14q12 deletions (five cases). We expand the mutational spectrum in patients with FOXG1-related encephalopathies and precise the core FOXG1 syndrome phenotype. Dysgenesis of the corpus callosum and dyskinesia are not always present in FOXG1-mutated patients. We believe that the FOXG1 gene should be considered in severely mentally retarded patients (no speech-language) with severe acquired microcephaly ( À4 to À6 SD) and few clinical features suggestive of Rett syndrome. Interestingly enough, three 14q12 deletions that do not include the FOXG1 gene are associated with phenotypes very reminiscent to that of FOXG1-mutation-positive patients. We physically mapped a putative long-range FOXG1-regulatory element in a 0.43 Mb DNA segment encompassing the PRKD1 locus. In fibroblast cells, a cis-acting regulatory sequence located more than 0.6 Mb away from FOXG1 acts as a silencer at the transcriptional level. These data are important for clinicians and for molecular biologists involved in the management of patients with severe encephalopathies compatible with a FOXG1-related phenotype.

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“…PKD1, also known as protein kinase C (PKC ), is the founding member of a the PKD family, which also includes PKD2 and PKD3/PKC (30). PKD1 has been identified as class IIa HDAC export kinase in cardiomyocytes and thymocytes (29,31,32). PKD has been implicated in diverse processes, such as, vesicular transport, metastasis, immune responses, apoptosis, and cell proliferation (30).…”

Section: Discussionmentioning

confidence: 99%

Control of endothelial cell proliferation and migration by VEGF signaling to histone deacetylase 7

Wang

Parra

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

227

200

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VEGF has been shown to regulate endothelial cell (EC) proliferation and migration. However, the nuclear mediators of the actions of VEGF in ECs have not been fully defined. We show that VEGF induces the phosphorylation of three conserved serine residues in histone deacetylase 7 (HDAC7) via protein kinase D, which promotes nuclear export of HDAC7 and activation of VEGF-responsive genes in ECs. Expression of a signal-resistant HDAC7 mutant protein in ECs inhibits proliferation and migration in response to VEGF. These results demonstrate that phosphorylation of HDAC7 serves as a molecular switch to mediate VEGF signaling and endothelial function.angiogenesis ͉ PKD1 ͉ MEF2 ͉ class II HDAC

show abstract

Protein kinase D directly phosphorylates histone deacetylase 5 via a random sequential kinetic mechanism

Cited by 57 publications

References 39 publications

Class IIa histone deacetylases: regulating the regulators

Class IIa histone deacetylases: regulating the regulators

14q12 and severe Rett-like phenotypes: new clinical insights and physical mapping of FOXG1-regulatory elements

Control of endothelial cell proliferation and migration by VEGF signaling to histone deacetylase 7

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