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PAP1 Pap1p

Pap1, poly(A) polymerase, LPIN1
The protein encoded by this gene can be bound and phosphorylated by the protooncogene PIM1 product, a serine/threonine protein kinase . This protein localizes in nuclear speckles containing the splicing factors, and has a role in pre-mRNA splicing. CBF1-interacting protein (CIR), a corepressor of CBF1, can also bind to this protein and effects alternative splicing. Mutations in this gene result in autosomal dominant retinitis pigmentosa-9. This gene has a pseudogene (GeneID: 441212), which is located in tandem array approximately 166 kb distal to this gene. [provided by RefSeq, Sep 2009] (from NCBI)
Top mentioned proteins: POLYMERASE, PAP, CAN, ACID, HAD
Papers using Pap1 antibodies
Lentiviral RNAs can use different mechanisms for translation initiation.
Nixon Douglas F., In PLoS ONE, 2007
... polyadenylation was performed with poly(A) polymerase (New England Biolabs) and tested by agarose ...
Crystal structure of the Cys2 activator-binding domain of protein kinase Cd in complex with phorbol ester
Meyer Tobias et al., In The Journal of Cell Biology, 1994
... , 250 mM NaCl, 0.25 mg/ml RNA, 250 mM ATP, and 5 units poly(A) polymerase (Life Technologies, Inc., Gaithersburg, MD) ...
Papers on Pap1
Oligoadenylation of 3' decay intermediates promotes cytoplasmic mRNA degradation in Drosophila cells.
Wahle et al., Halle, Germany. In Rna, Feb 2016
RNAi experiments showed that the oligoadenylated RNA fragments were intermediates of exosomal decay and the noncanonical poly(A) polymerase Trf4-1 was mainly responsible for A addition.
The polyadenylation complex of Trypanosoma brucei: characterization of the functional poly(A) polymerase.
Preußer et al., Gießen, Germany. In Rna Biol, Feb 2016
To characterize the catalytic core of the polyadenylation complex in T. brucei, we first identified the poly(A) polymerase [Tb927.7.3780] as the major functional, nuclear-localized enzyme in trypanosomes.
Regulation of the antioxidant system in cells of the fission yeast Schizosaccharomyces pombe after combined treatment with patulin and citrinin.
Pesti et al., Pécs, Hungary. In Toxicon, Feb 2016
The pattern of the ROS was the same as that induced by CTN (Máté et al., 2014), while the presence of PAT in the PAT+CTN combination treatment modified the activities of the antioxidant system (Papp et al., 2012) in comparison with the individual PAT or CTN treatment, suggesting toxin-specific regulation of glutathione and the enzymes of the antioxidant system and the possibility that the transcription factor (pap1 and atf1) -regulated processes might be influenced directly by ROS.
Overexpression of SREBP1 (sterol regulatory element binding protein 1) promotes de novo fatty acid synthesis and triacylglycerol accumulation in goat mammary epithelial cells.
Bionaz et al., China. In J Dairy Sci, Jan 2016
Among genes related to milk fat synthesis and lipid droplet formation, only LPIN1 and DGAT1 were upregulated by Ad-nSREBP1.
Three indel variants in chicken LPIN1 exon 6/flanking region are associated with performance and carcass traits.
Huang et al., Zhengzhou, China. In Br Poult Sci, Dec 2015
LPIN1 is a Mg(2+)-dependent phosphatidic acid phosphatase.
Veterinary Medicine and Omics (Veterinomics): Metabolic Transition of Milk Triacylglycerol Synthesis in Sows from Late Pregnancy to Lactation.
Liao et al., Guangzhou, China. In Omics, Oct 2015
Robust upregulation with high relative mRNA abundance was evident during lactation for genes associated with FA uptake (VLDLR, LPL, CD36), FA activation (ACSS2, ACSL3), and intracellar transport (FABP3), de novo FA synthesis (ACACA, FASN), FA elongation (ELOVL1), FA desaturation (SCD, FADS1), TAG synthesis (GPAM, AGPAT1, LPIN1, DGAT1), lipid droplet formation (BTN2A1, XDH, PLIN2), and transcription factors and nuclear receptors (SREBP1, SCAP, INSIG1/2).
Acute rhabdomyolysis and inflammation.
de Lonlay et al., Paris, France. In J Inherit Metab Dis, Jul 2015
In addition, our studies on lipin-1 (LPIN1) deficiency raise the possibility that several diseases involved in rhabdomyolysis implicate pro-inflammatory cytokines and may even represent primarily pro-inflammatory diseases.
Inborn errors of cytoplasmic triglyceride metabolism.
Mitchell et al., Montréal, Canada. In J Inherit Metab Dis, 2015
We discuss known inborn errors of CTGM, including deficiencies of: AGPAT2 (a form of generalized lipodystrophy), LPIN1 (childhood rhabdomyolysis), LPIN2 (an inflammatory condition, Majeed syndrome, described elsewhere in this issue), DGAT1 (protein loosing enteropathy), perilipin 1 (partial lipodystrophy), CGI-58 (gene ABHD5, neutral lipid storage disease (NLSD) with ichthyosis and "Jordan's anomaly" of vacuolated polymorphonuclear leukocytes), adipose triglyceride lipase (ATGL, gene PNPLA2, NLSD with myopathy, cardiomyopathy and Jordan's anomaly), hormone-sensitive lipase (HSL, gene LIPE, hypertriglyceridemia, and insulin resistance).
Lipin-1 regulates autophagy clearance and intersects with statin drug effects in skeletal muscle.
Reue et al., Los Angeles, United States. In Cell Metab, 2014
LPIN1 encodes lipin-1, a phosphatidic acid phosphatase (PAP) enzyme that catalyzes the dephosphorylation of phosphatidic acid to form diacylglycerol.
Poly(A) polymerase (PAP) diversity in gene expression--star-PAP vs canonical PAP.
Laishram, Thiruvananthapuram, India. In Febs Lett, 2014
The canonical PAP, PAPα, was considered the only nuclear PAP involved in general polyadenylation of mRNAs.
Cytoplasmic RNA: a case of the tail wagging the dog.
Norbury, Oxford, United Kingdom. In Nat Rev Mol Cell Biol, 2013
In recent years, surprising roles for cytoplasmic poly(A) polymerase-related enzymes that add uridylyl, rather than adenylyl, residues to RNA 3' ends have also emerged.
The interplay of Hfq, poly(A) polymerase I and exoribonucleases at the 3' ends of RNAs resulting from Rho-independent termination: A tentative model.
Hajnsdorf et al., Paris, France. In Rna Biol, 2013
In Escherichia coli, most accessible 3' RNA extremities are believed to be potential targets of poly(A) polymerase I.
RNAi triggered by specialized machinery silences developmental genes and retrotransposons.
Grewal et al., Bethesda, United States. In Nature, 2013
We show that the generation of siRNAs and heterochromatin assembly by RNAi is triggered by a mechanism involving the canonical poly(A) polymerase Pla1 and an associated RNA surveillance factor Red1, which also activate the exosome.
NF-E2-related factor 1 (Nrf1) serves as a novel regulator of hepatic lipid metabolism through regulation of the Lipin1 and PGC-1β genes.
Yamamoto et al., Sendai, Japan. In Mol Cell Biol, 2012
Nrf1 binds to the antioxidant response elements (AREs) in regulatory regions of the Lipin1 and PGC-1beta genes and the binding of Nrf1 to the AREs activates reporter gene transcription.
The transcription factors Pap1 and Prr1 collaborate to activate antioxidant, but not drug tolerance, genes in response to H2O2.
Hidalgo et al., Barcelona, Spain. In Nucleic Acids Res, 2012
The ability of Pap1 to bind and activate drug tolerance promoters is independent on Prr1, whereas its affinity for the antioxidant promoters is significantly enhanced upon association with Prr1.
Fatal rhabdomyolysis in 2 children with LPIN1 mutations.
de Lonlay et al., Paris, France. In J Pediatr, 2012
LPIN1 mutations should be considered in any child presenting with severe rhabdomyolysis.
LPIN1 rs13412852 polymorphism in pediatric nonalcoholic fatty liver disease.
Nobili et al., Milano, Italy. In J Pediatr Gastroenterol Nutr, 2012
Lipin1 rs13412852 single nucleotide polymorphism is associated with the severity of liver damage and fibrosis progression in pediatric patients with histological NAFLD.
Novel interactions at the essential N-terminus of poly(A) polymerase that could regulate poly(A) addition in Saccharomyces cerevisiae.
Moore et al., Boston, United States. In Febs Lett, 2012
results suggest a novel mechanism for controlling Pap1 activity, and possible models invoking these newly-discovered interactions are discussed.
Response to Brosch et al.
Patti et al., Boston, United States. In Cell Metab, 2012
Brosch performed RT-PCR in liver samples from 13 lean and 34 obese individuals, finding no differences in SFRS10 or LPIN1 expression.
Expression of the splicing factor gene SFRS10 is reduced in human obesity and contributes to enhanced lipogenesis.
Patti et al., Boston, United States. In Cell Metab, 2011
reduced expression of SFRS10, as observed in tissues from obese humans, alters LPIN1 splicing, induces lipogenesis, and therefore contributes to metabolic phenotypes associated with obesity.
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