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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Pleckstrin homology-like domain, family A, member 3

Tih1, PHLDA3
Top mentioned proteins: p53, Akt, IPL, PA26, V1a
Papers on Tih1
Hypoxia-induced p53 modulates both apoptosis and radiosensitivity via AKT.
Hammond et al., In J Clin Invest, Jun 2015
Evaluation of hypoxia-induced transcripts in multiple cell lines identified a group of genes that are hypoxia-inducible proapoptotic targets of p53, including inositol polyphosphate-5-phosphatase (INPP5D), pleckstrin domain-containing A3 (PHLDA3), sulfatase 2 (SULF2), B cell translocation gene 2 (BTG2), cytoplasmic FMR1-interacting protein 2 (CYFIP2), and KN motif and ankyrin repeat domains 3 (KANK3).
PHLDA3 overexpression in hepatocytes by endoplasmic reticulum stress via IRE1-Xbp1s pathway expedites liver injury.
Kim et al., Seoul, South Korea. In Gut, Jun 2015
This study investigated the role of pleckstrin homology-like domain, family A, member-3 (PHLDA3), in hepatocyte death caused by ER stress and the regulatory basis.
Low PHLDA3 expression in oesophageal squamous cell carcinomas is associated with poor prognosis.
Kato et al., Tochigi, Japan. In Anticancer Res, Feb 2015
Pleckstrin homology-like domain, family A, member 3 (PHLDA3) has been identified as a direct target gene of p53 and as a potent inhibitor of Akt activation.
PHLDA3 is a novel tumor suppressor of pancreatic neuroendocrine tumors.
Nakagama et al., Tokyo, Japan. In Proc Natl Acad Sci U S A, 2014
We report here that the genomic region of the PHLDA3 gene undergoes loss of heterozygosity (LOH) at a remarkably high frequency in human PanNETs, and this genetic change is correlated with disease progression and poor prognosis.
IPH-926 lobular breast cancer cells harbor a p53 mutant with temperature-sensitive functional activity and allow for profiling of p53-responsive genes.
Lehmann et al., Hannover, Germany. In Lab Invest, 2012
These genes included CDKN1A, MDM2 and PHLDA3, a recently described p53-inducible inhibitor of AKT.
Proposed megakaryocytic regulon of p53: the genes engaged to control cell cycle and apoptosis during megakaryocytic differentiation.
Papoutsakis et al., Evanston, United States. In Physiol Genomics, 2012
Among substantially downregulated p53 targets in p53-KD megakaryocytes were cell cycle regulators CDKN1A (p21) and PLK2, proapoptotic FAS, TNFRSF10B, CASP8, NOTCH1, TP53INP1, TP53I3, DRAM1, ZMAT3 and PHLDA3, DNA-damage-related RRM2B and SESN1, and actin component ACTA2, while antiapoptotic CKS1B, BCL2, GTSE1, and p53 family member TP63 were upregulated in p53-KD cells.
Global methylation profiling for risk prediction of prostate cancer.
Donkena et al., Rochester, United States. In Clin Cancer Res, 2012
Validation of genes by pyrosequencing from group 1 (GSTP1, HIF3A, HAAO, and RARĪ²), group 2 (CRIP1, FLNC, RASGRF2, RUNX3, and HS3ST2), group 3 (PHLDA3, RASGRF2, and TNFRSF10D), and group 4 (BCL11B, POU3F3, and RASGRF2) confirmed the microarray results.
Expressional and mutational analysis of PHLDA3 gene in common human cancers.
Lee et al., In Pathology, 2011
findings indicate somatic mutation of PHLDA3 is rare in common cancer types; PHLDA3 expression was lost in 22% of prostate cancers; these results indicate that PHLDA3 are altered in prostate cancers by loss of expression
Physiological regulation of Akt activity and stability.
Hung et al., In Am J Transl Res, 2009
This literature review details findings of those reports and others relevant to the regulation of Akt activation by its upstream kinases, with a focus on mammalian target of rapamycin complexes (mTORCs) and inactivation by PHLDA3 and the protein phosphatases PP2A and pleckstrin homology domain leucine-rich repeat protein phosphatase (PHLPP).
Microarray analysis of prothrombin knockdown in zebrafish.
Jagadeeswaran et al., San Antonio, United States. In Blood Cells Mol Dis, 2009
One particular gene, phlda3, was at least eleven fold upregulated, and in situ hybridization revealed expansion of phlda3 expression in the central nervous system, branchial arches, and head endoderm in knockdown embryos.
RVB1/RVB2: running rings around molecular biology.
Dutta et al., Charlottesville, United States. In Mol Cell, 2009
RVB1/RVB2 (also known as Pontin/Reptin, TIP49/TIP48, RuvbL1/RuvbL2, ECP54/ECP51, INO80H/INO80J, TIH1/TIH2, and TIP49A/TIP49B) are two highly conserved members of the AAA+ family that are present in different protein and nucleoprotein complexes.
PH domain-only protein PHLDA3 is a p53-regulated repressor of Akt.
Taya et al., Tokyo, Japan. In Cell, 2009
Study identifies PHLDA3 as a p53 target gene that encodes a PH domain-only protein and finds that PHLDA3 competes with the PH domain of Akt for binding of membrane lipids, inhibiting Akt translocation to the cellular membrane and activation.
A p53-dominant transcriptional response to cisplatin in testicular germ cell tumor-derived human embryonal carcinoma.
Spinella et al., United States. In Oncogene, 2005
Several of these gene products, including FAS, TRAILR3, PHLDA3, LRDD, and IER3 are previously implicated in the apoptotic death receptor pathway, while others including SESN1, FDXR, PLK3, and DDIT4 are known mediators of reactive oxygen species generation.
Phosphoinositide binding by the pleckstrin homology domains of Ipl and Tih1.
Tycko et al., New York City, United States. In J Biol Chem, 2003
Ipl and Tih1 are bona fide PH domain proteins, with broad specificity and moderate affinity for PIPs.
Placental overgrowth in mice lacking the imprinted gene Ipl.
Tycko et al., New York City, United States. In Proc Natl Acad Sci U S A, 2002
We constructed two lines of mice with germ-line deletions of this gene (Ipl(neo) and Ipl(loxP)) and another line deleted for the similar but nonimprinted gene Tih1.
A novel pleckstrin homology-related gene family defined by Ipl/Tssc3, TDAG51, and Tih1: tissue-specific expression, chromosomal location, and parental imprinting.
Tycko et al., New York City, United States. In Mamm Genome, 1999
Here we describe another gene, Tih1 (TDAG/Ipl homologue 1), with equivalent sequence similarity to Ipl.
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