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Post-GPI attachment to proteins 2

FRAG1, PGAP2, Post-GPI-Attachment to Proteins 2
stimulates transforming activity and autophosphorylation of the receptor [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: ACID, Aps, CD59, FGFR2, PIG-L
Papers on FRAG1
Differences in transcript abundance of genes on BTA15 located within a region associated with gain in beef steers.
Freetly et al., United States. In Gene, Dec 2015
The genes evaluated were two olfactory receptor-like genes (LOC525033 and LOC618173), RRM1, STIM1, RHOG, PGAP2, and NUP98.
Comparative Haploid Genetic Screens Reveal Divergent Pathways in the Biogenesis and Trafficking of Glycophosphatidylinositol-Anchored Proteins.
Shen et al., Boulder, United States. In Cell Rep, Jul 2015
PIGN, PGAP2, and PIGF, which encode GPI anchor-modifying enzymes, were selectively isolated in the CD59 screen, suggesting that GPI anchor composition significantly influences the biogenesis of GPI-APs in a substrate-dependent manner.
Mutations in PIGL in a patient with Mabry syndrome.
Aoki et al., Sendai, Japan. In Am J Med Genet A, Apr 2015
Recent studies have revealed mutations in PIGV, PIGW, PIGO, PGAP2, and PGAP3 (genes that encode molecules of the glycosylphosphatidylinositol (GPI)-anchor biosynthesis pathway) in patients with HPMRS.
Delineation of PIGV mutation spectrum and associated phenotypes in hyperphosphatasia with mental retardation syndrome.
Krawitz et al., Berlin, Germany. In Eur J Hum Genet, 2014
Three different genes of the glycosylphosphatidylinositol anchor synthesis pathway, PIGV, PIGO, and PGAP2, have recently been implicated in hyperphosphatasia-mental retardation syndrome (HPMRS), also known as Mabry syndrome, a rare autosomal recessive form of intellectual disability.
Mutations in PGAP3 impair GPI-anchor maturation, causing a subtype of hyperphosphatasia with mental retardation.
Krawitz et al., Ōsaka, Japan. In Am J Hum Genet, 2014
Taken together with recent data on PGAP2, these results confirm the importance of the later GPI-anchor remodelling steps for normal neuronal development.
PIGO mutations in intractable epilepsy and severe developmental delay with mild elevation of alkaline phosphatase levels.
Saitsu et al., Yokohama, Japan. In Epilepsia, 2014
Among them, mutations in PIGV and PIGO, which are involved in the late stages of GPI-anchor synthesis, and PGAP2, which is involved in fatty-acid GPI-anchor remodeling, are all causative for hyperphosphatasia with mental retardation syndrome (HPMRS).
Hypomorphic mutations in PGAP2, encoding a GPI-anchor-remodeling protein, cause autosomal-recessive intellectual disability.
Abou Jamra et al., Copenhagen, Denmark. In Am J Hum Genet, 2013
PGAP2 encodes a protein involved in remodeling the glycosylphosphatidylinositol (GPI) anchor in the Golgi apparatus.
PGAP2 mutations, affecting the GPI-anchor-synthesis pathway, cause hyperphosphatasia with mental retardation syndrome.
Horn et al., Berlin, Germany. In Am J Hum Genet, 2013
We developed a diagnostic gene panel for targeting all known genes encoding proteins in the GPI-anchor-synthesis pathway to screen individuals matching these features, and we detected three missense mutations in PGAP2, c.46C>T, c.380T>C, and c.479C>T, in two unrelated individuals with hyperphosphatasia with mental retardation syndrome (HPMRS).
Enhanced response of T lymphocytes from Pgap3 knockout mouse: Insight into roles of fatty acid remodeling of GPI anchored proteins.
Murakami et al., Japan. In Biochem Biophys Res Commun, 2012
Fatty acid remodeling of GPI-APs in the Golgi apparatus is required for their efficient association with lipid rafts, i.e., the unsaturated fatty acid at the sn-2 position of the PI moiety is exchanged for the saturated fatty acid by PGAP2 and PGAP3.
Disialogangliosides and TNFα alter gene expression for cytokines and chemokines in primary brain cell cultures.
Irwin et al., El Paso, United States. In Neurochem Res, 2012
The expression of FGF receptor activating protein 1 (FRAG1) and interleukin-3 receptor alpha (IL3RA) was down-regulated by GD3.
Dynamic regulation of PCNA ubiquitylation/deubiquitylation.
Myung et al., Bethesda, United States. In Febs Lett, 2011
Studies indicate that USP1 and ELG1 as regulators of PCNA ubiquitylation.
Predisposition to cancer caused by genetic and functional defects of mammalian Atad5.
Myung et al., Bethesda, United States. In Plos Genet, 2011
loss-of-function mutations in mammalian Atad5 are sufficient to cause genomic instability and tumorigenesis.
Osmolytes contribute to pH homeostasis of Escherichia coli.
Slonczewski et al., United States. In Plos One, 2009
The wild-type strain Frag1 was exposed to rapid external acidification by HCl addition.
DNA damage responses by human ELG1 in S phase are important to maintain genomic integrity.
Myung et al., Bethesda, United States. In Cell Cycle, 2009
Human ELG1 protein is stabilized and localized to form foci at sites of stalled DNA replications that are different from DNA double strand breaks foci.
Fluorescence approach to evaluating conformational changes upon binding of beta-spectrin ankyrin-binding domain mutants with the lipid bilayer.
Langner et al., Wrocław, Poland. In Gen Physiol Biophys, 2009
In the present study, in order to better understand the character of binding, a more detailed investigation of the interactions between the beta-spectrin fragments corresponding to the truncated mutants of the ankyrin-binding domain (Frag1 and Frag3) and liposomes of different compositions were carried out.
Cyclopropane fatty acids improve Escherichia coli survival in acidified minimal media by reducing membrane permeability to H+ and enhanced ability to extrude H+.
Ross et al., Hobart, Australia. In Res Microbiol, 2008
The physiological role of cyclopropane fatty acids (CFAs) in acid stress resistance was studied by in situ microelectrode H+ flux measurements of Escherichia coli Frag1 and its isogenic CFA-deficient mutant JBM 1.
Saccharomyces cerevisiae CWH43 is involved in the remodeling of the lipid moiety of GPI anchors to ceramides.
Jigami et al., Ibaraki, Japan. In Mol Biol Cell, 2007
Our results also indicate that mouse FRAG1 and C130090K23, which are homologous to Cwh43-N and -C, respectively, share these activities.
CWH43 is required for the introduction of ceramides into GPI anchors in Saccharomyces cerevisiae.
Conzelmann et al., Fribourg, Switzerland. In Mol Microbiol, 2007
CWH43 of yeast is homologous to PGAP2, a gene that recently was implicated in a similar deacylation reacylation cycle of GPI proteins in mammalian cells, where PGAP2 is required for the reacylation of monoradylglycerol-type GPI anchors.
PGAP2 is essential for correct processing and stable expression of GPI-anchored proteins.
Maeda et al., Suita, Japan. In Mol Biol Cell, 2006
results demonstrate that PGAP2 is involved in the processing of GPI-APs required for their stable expression at the cell surface
Frag1, a homolog of alternative replication factor C subunits, links replication stress surveillance with apoptosis.
Furukawa et al., Tochigi, Japan. In Proc Natl Acad Sci U S A, 2005
The Frag1 signal pathway, by linking replication stress surveillance with apoptosis induction, plays a central role in determining whether DNA damage is compatible with cell survival or whether it requires cell elimination by apoptosis.
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