Caenorhabditis elegans PIAK, a phospholipid-independent kinase that activates the AKT/PKB survival kinase.

Caenorhabditis elegans PIAK, a phospholipid-independent kinase that activates the AKT/PKB survival kinase. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Caenorhabditis elegans PIAK, a phospholipid-independent kinase that activates the AKT/PKB survival kinase. Abstract Text:

Phospholipid-dependent kinase 1 (PDK 1) is a 3'-phospholipid-responsive serine/threonine kinase that plays a critical role in cell survival by phosphorylating and activating the anti-apoptotic AKT/PKB kinase. While PDK 1 is clearly an important component of the cell survival machinery, the potential for phospholipid-independent activation of the AKT/PKB survival pathway has not been extensively examined at the molecular level. We have identified a second form of PDK 1 in the nematode Caenorhabditis elegans that we have termed PIAK (phospholipid-independent AKT/PKB kinase). PIAK is highly homologous to C. elegans and mammalian PDK 1 with the exception that the novel kinase lacks a phospholipid binding pleckstrin homology domain. The domain structure of PIAK suggests that it might be a phospholipid-independent kinase, and PIAK phosphorylates mammalian AKT/PKB at the activating Thr(308) residue in the presence of the phosphatidylinositol (PI) 3-kinase inhibitors as well as in the absence of growth factors. In addition, PIAK is capable of inducing the phospholipid-independent, AKT/PKB-induced phosphorylation of the AFX-type forkhead transcription factor, resulting in its cytoplasmic localization. Because the nuclear localization of this transcription factor induces an apoptotic state, this PIAK-mediated cytoplasmic sequestration allows for cell survival. Finally, PIAK activity appears to be induced by various inhibitors of cell cycle G(1) progression. These data suggest an alternate, phosphatidylinositol 3-kinase-independent mechanism for the activation of the AKT/PKB survival pathway that may be utilized during periods of cellular quiescence.

Caenorhabditis elegans PIAK, a phospholipid-independent kinase that activates the AKT/PKB survival kinase. Publishing Authors By Initials

For similar proteins: transcription factors research abstracts see: proteins: transcription factors research

PUBMED ID PMID:

MEDLINE DATE:

Caenorhabditis elegans PIAK, a phospholipid-independent kinase that activates the AKT/PKB survival kinase. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: The Journal of biological chemistry

VOLUME: 276

Page Numbers: 20323-9

Journal Abbreviation: J. Biol. Chem.

ISSN: 0021-9258

DAY: 23

MONTH: 03

YEAR: 2001

Caenorhabditis elegans PIAK, a phospholipid-independent kinase that activates the AKT/PKB survival kinase. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2985121

Caenorhabditis elegans PIAK, a phospholipid-independent kinase that activates the AKT/PKB survival kinase. Keywords Mesh Terms:

KEYWORDS: Transcription Factors

MESH TERMS: metabolism

Chemical & Substance for Abstract: Caenorhabditis elegans PIAK, a phospholipid-independent kinase that activates the AKT/PKB survival kinase. Information

Substance Name: Protein-Serine-Threonine Kinases

Registry Number: EC 2.7.11.1

Grant and Affiliation Information for Caenorhabditis elegans PIAK, a phospholipid-independent kinase that activates the AKT/PKB survival kinase.

AFFILIATION: Department of Molecular Oncology, Genentech, Inc., South San Francisco, California 94080.

Country: United States

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: J Biol Chem

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Caenorhabditis elegans PIAK, a phospholipid-independent kinase that activates the AKT/PKB survival kinase Related Publications

• A developmental study on the effect of stimulus rate on the auditory evoked brain-stem response.
• Activation of proMMP-2 and Src by HHV8 vGPCR in human pulmonary arterial endothelial cells.
• Application of transcranial Doppler sonography in children with acute neurologic events due to primary cerebral and West Nile vasculitis.
• Biophysical hematology and medical applications. UCLA 12-724.
• Biophysical hematology and medical applications. UCLA-12-686.
• Caenorhabditis elegans PIAK, a phospholipid-independent kinase that activates the AKT/PKB survival kinase.
• Effects of hypoxic-ischemic encephalopathy and whole-body hypothermia on neonatal auditory function: a pilot study.
• Essential progressive atrophy of the iris.
• Fibrous histiocytoma of the eyelid obliterating the punctum and the canaliculus.
• Histone Deacetylase 6 Regulates TGF-{beta}1-mediated Epithelial-Mesenchymal Transition.
• Human cytotoxic T cell clones directed against herpes simplex virus-infected cells. IV. Recognition and activation by cloned glycoproteins gB and gD.
• Over-expression of PDGF-C using a lung specific promoter results in abnormal lung development.
• Postnatal lead effects on the development of visual spatial acuity in rhesus monkeys (Macaca Mulatta).
• Requirement of HDAC6 for Transforming Growth Factor-{beta}1-induced Epithelial-Mesenchymal Transition.
• The forkhead transcription factor AFX activates apoptosis by induction of the BCL-6 transcriptional repressor.
• The forkhead transcription factor FOXO4 induces the down-regulation of hypoxia-inducible factor 1 alpha by a von Hippel-Lindau protein-independent mechanism.
• Transforming Growth Factor-{beta}1 Induces Heparan Sulfate 6-O-Endosulfatase 1 Expression in Vitro and in Vivo.