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Nuclear prelamin A recognition factor

NARF, TRIM2, nuclear prelamin A recognition factor, HSD4, IOP2
Several proteins have been found to be prenylated and methylated at their carboxyl-terminal ends. Prenylation was initially believed to be important only for membrane attachment. However, another role for prenylation appears to be its importance in protein-protein interactions. The only nuclear proteins known to be prenylated in mammalian cells are prelamin A- and B-type lamins. Prelamin A is farnesylated and carboxymethylated on the cysteine residue of a carboxyl-terminal CaaX motif. This post-translationally modified cysteine residue is removed from prelamin A when it is endoproteolytically processed into mature lamin A. The protein encoded by this gene binds to the prenylated prelamin A carboxyl-terminal tail domain. It may be a component of a prelamin A endoprotease complex. The encoded protein is located in the nucleus, where it partially colocalizes with the nuclear lamina. It shares limited sequence similarity with iron-only bacterial hydrogenases. Alternatively spliced transcript variants encoding different isoforms have been identified for this gene, including one with a novel exon that is generated by RNA editing. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: HAD, CAN, POLYMERASE, Ubiquitin, OUT
Papers on NARF
ALS5/SPG11/KIAA1840 mutations cause autosomal recessive axonal Charcot-Marie-Tooth disease.
Orlacchio et al., Roma, Italy. In Brain, Jan 2016
Besides, we screened for all the known genes related to axonal autosomal recessive Charcot-Marie-Tooth disease (CMT2A2/HMSN2A2/MFN2, CMT2B1/LMNA, CMT2B2/MED25, CMT2B5/NEFL, ARCMT2F/dHMN2B/HSPB1, CMT2K/GDAP1, CMT2P/LRSAM1, CMT2R/TRIM2, CMT2S/IGHMBP2, CMT2T/HSJ1, CMTRID/COX6A1, ARAN-NM/HINT and GAN/GAN), for the genes related to autosomal recessive hereditary spastic paraplegia with thin corpus callosum and axonal peripheral neuropathy (SPG7/PGN, SPG15/ZFYVE26, SPG21/ACP33, SPG35/FA2H, SPG46/GBA2, SPG55/C12orf65 and SPG56/CYP2U1), as well as for the causative gene of peripheral neuropathy with or without agenesis of the corpus callosum (SLC12A6).
Estrogenic and anti-estrogenic influences in cultured brown trout hepatocytes: Focus on the expression of some estrogen and peroxisomal related genes and linked phenotypic anchors.
Rocha et al., Porto, Portugal. In Aquat Toxicol, Dec 2015
The mRNA levels of the estrogenic targets (ERα, ERβ-1 and vitellogenin A-VtgA) and the peroxisome structure/function related genes (catalase, urate oxidase-Uox, 17β-hydroxysteroid dehydrogenase 4-17β-HSD4, peroxin 11α-Pex11α and PPARα) were analyzed by real-time polymerase chain reaction (RT-PCR).
MicroRNA-145 targets TRIM2 and exerts tumor-suppressing functions in epithelial ovarian cancer.
Xu et al., Zhenjiang, China. In Gynecol Oncol, Dec 2015
Furthermore, computational algorithm combined with luciferase reporter assays identified TRIM2 as the direct target of miR-145 in EOC cells.
DLVO and XDLVO calculations for bacteriophage MS2 adhesion to iron oxide particles.
Kim et al., Seoul, South Korea. In J Contam Hydrol, Oct 2015
In this study, batch experiments were performed to examine the adhesion of bacteriophage MS2 to three iron oxide particles (IOP1, IOP2 and IOP3) with different particle properties.
Exome sequencing reveals homozygous TRIM2 mutation in a patient with early onset CMT and bilateral vocal cord paralysis.
Harel et al., Houston, United States. In Hum Genet, Jun 2015
TRIM2, encoding a ligase that ubiquitinates the neurofilament light chain, was recently associated with early-onset neuropathy in a single patient.
Laminopathy-inducing mutations reduce nuclear import of expressed prelamin A.
Hübner et al., Würzburg, Germany. In Int J Biochem Cell Biol, 2014
In the case of the full length prelamin A mutants R419C and L421P altered subcellular localization and reduced lamina incorporation were detected, with the prelamin A-binding protein Narf being redistributed into R419-containing aggregates.
Expression, purification, crystallization and preliminary X-ray diffraction analysis of the C-terminal NHL domain of human TRIM2.
Li et al., Beijing, China. In Acta Crystallogr Sect F Struct Biol Commun, 2014
The tripartite motif-containing protein 2 (TRIM2) functions as an E3 ubiquitin ligase.
Bortezomib inhibits STAT5-dependent degradation of LEF-1, inducing granulocytic differentiation in congenital neutropenia CD34(+) cells.
Skokowa et al., In Blood, 2014
We demonstrated that constitutively active STAT5a (caSTAT5a) inhibited LEF-1-dependent autoregulation of the LEF-1 gene promoter by binding to the LEF-1 protein, recruiting Nemo-like kinase and the E3 ubiquitin-ligase NARF to LEF-1, leading to LEF-1 ubiquitination and a reduction in LEF-1 protein levels.
Dietary strategy to repair plasma membrane after brain trauma: implications for plasticity and cognition.
Gomez-Pinilla et al., Los Angeles, United States. In Neurorehabil Neural Repair, 2014
RESULTS: Fluid percussion injury reduced DHA levels as well as levels of enzymes involved in the metabolism of DHA such as FADS2 and 17β-HSD4 and elevated levels of markers of lipid peroxidation such as 4-hydroxy-2-nonenal (4-HNE) and 4-hydroxy-2-hexenal (4-HHE).
Differential expression of tripartite motif-containing family in normal human dermal fibroblasts in response to porcine endogenous retrovirus infection.
Twardoch et al., Sosnowiec, Poland. In Folia Biol (praha), 2013
Nine (TRIM1, TRIM2, TRIM5, TRIM14, TRIM16, TRIM18, TRIM22, TRIM27 and TRIM31) statistically significantly differentially expressed genes were found (P < 0.05, one-way ANOVA).
Exercise facilitates the action of dietary DHA on functional recovery after brain trauma.
Gomez-Pinilla et al., Los Angeles, United States. In Neuroscience, 2013
FPI reduced the enzymes acyl-CoA oxidase 1 (Acox1) and 17β-hydroxysteroid dehydrogenase type 4 (17β-HSD4), and the calcium-independent phospholipases A2 (iPLA2), which are involved in metabolism of membrane phospholipids.
Deficiency of the E3 ubiquitin ligase TRIM2 in early-onset axonal neuropathy.
Tyynismaa et al., Helsinki, Finland. In Hum Mol Genet, 2013
Here, we report compound heterozygous mutations in the tripartite motif containing 2 (TRIM2) gene in a patient with childhood-onset axonal neuropathy, low weight and small muscle mass.
Diagnostic SOX10 gene signatures in salivary adenoid cystic and breast basal-like carcinomas.
Yarbrough et al., New Haven, United States. In Br J Cancer, 2013
Diagnostic significance of several conserved elements of the SOX10 signature (MIA, TRIM2, ROPN1, and ROPN1B) was validated on BBC cell lines.
Effects of polar oil related hydrocarbons on steroidogenesis in vitro in H295R cells.
Meier et al., Bergen, Norway. In Chemosphere, 2013
Endpoints include hormone (cortisol, estradiol, progesterone, testosterone) production at the functional level and key genes for steroidogenesis (17β-HSD1, 17β-HSD4, 3β-HSD2, ACTHR, CYP11A1, CYP11B1, CYP11B2, CYP17, CYP19, CYP21, DAX1, EPHX, HMGR, SF1, STAR) and metabolism (CYP1A) at the molecular level.
Effect of topical application of tetracaine on intraocular pressure in dogs: preliminary results.
Rosolen et al., Saintes, France. In J Fr Ophtalmol, 2013
For group 1, IOP1 mean (SD), IOP2 mean (SD), IOP3 mean (SD) and IOP4 mean (SD) were 14.6 (2.2) mmHg, 11.3 (3.2) mmHg, 14.4 (2.2) mmHg and 13.5 (3.9) mmHg respectively, while in group 2, IOP1 mean (SD), IOP2 mean (SD), IOP3 mean (SD) and IOP4 mean (SD) were 14.2 (3.8) mmHg, 9.5 (3.7) mmHg, 13.5 (2.8) mmHg and 13.0 (3.8) mmHg respectively.
Target gene repression mediated by miRNAs miR-181c and miR-9 both of which are down-regulated by amyloid-β.
Götz et al., Sydney, Australia. In J Mol Neurosci, 2012
TRIM2 is repressed by miR-9 and -181c, either alone or in combination.
Identification of a novel Bcl-2-interacting mediator of cell death (Bim) E3 ligase, tripartite motif-containing protein 2 (TRIM2), and its role in rapid ischemic tolerance-induced neuroprotection.
Meller et al., Atlanta, United States. In J Biol Chem, 2011
a role for TRIM2 in mediating the p42/p44 MAPK-dependent ubiquitination of Bim in rapid ischemic tolerance.
The E3-ubiquitin ligase TRIM2 regulates neuronal polarization.
Schwamborn et al., Münster, Germany. In J Neurochem, 2011
Trim2 has an important function in the regulation of axon outgrowth during development.
Beyond DNA: RNA editing and steps toward Alu exonization in primates.
Schmitz et al., Münster, Germany. In J Mol Biol, 2008
Data suggest that gorilla, chimpanzee, and human nuclear prelamin A recognition factor genes exemplify the versatile interplay of pre- and posttranscriptional modifications leading to novel genetic potential.
Deficiency in ubiquitin ligase TRIM2 causes accumulation of neurofilament light chain and neurodegeneration.
Gruss et al., Göttingen, Germany. In Proc Natl Acad Sci U S A, 2008
TRIM2 is an ubiquitin ligase and point to a mechanism regulating neurofilament light subunit metabolism through an ubiquitination pathway that, if deregulated, triggers neurodegeneration
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