Figure 3. Reduced fat absorption of Arfrp1<sup>vil−/−</sup> mice. (A) A fat tolerance test was performed in 5 h fasted Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup>

Slides:

Advertisements

Similar presentations

Lipoprotein Metabolism And Disorders

Advertisements

LIPOPROTEIN METABOLISM

Figure 3. (A) Effect of the ON length on the HTT mRNA knockdown efficiency. LNA/DNA CAG 10- to 19-mer PS ONs were transfected at 100 nM concentration into.

Figure 1. DNA damage induced by 5-azadC

Figure 2. BRCA2–RAD51 complexes organize into filament-like structures

Figure 1. Gene expression analysis

Figure 2. Number of cases required in a Mendelian randomization analysis with a binary outcome and a single instrumental variable for 80% power with a.

J Exp Bot. 2017;68(17): doi: /jxb/erx352

Figure 5 ISOX and vorinostat partially restore splicing pattern in DM1 patient-derived fibroblasts. (A) ISOX and vorinostat partially rescue mis-splicing.

Fig. 1 Comparison of the rLH/hCG effects on cGMP levels in mouse ovary in vivo and cultured POFs in vitro. A) Comparison of the rLH/hCG effects on cGMP.

Fig. 1. Adhiron coding region and phagemid vector

Figure 1. Inhibition of GSK3β reduces MiR biogenesis through repression of pri-MiR processing. (A) qRT-PCR analysis of miR-27a, miR-23a, miR-24, miR-141.

From: Dasatinib as a treatment for Duchenne muscular dystrophy

Figure 3: MetaLIMS sample input.

Figure 1 An overview of the study design.

Figure 2. The graphic integration of CNAs with altered expression genes in lung AD and SCC. The red lines represent the amplification regions for CNA and.

Fig. 1. Trial structure for the experimental task.

Fig. 1 Nodes in a conceptual knowledge graph

Figure 1: Pneumomediastinum and subcutaneous emphysema as indicated by the arrows. From: Pneumomediastinum and subcutaneous emphysema after successful.

Figure 1. drb7.2 mutant plants display altered accumulation of endoIR-siRNA. Wild-type (Col-0) and drb7.2 mutant plants were subjected to high throughput.

Figure 1. DNMT3A interacts with the histone deiminase PADI4

Figure 1. Example of a template search of expression data: screenshot of the ‘SpellDataSet→SpellScore→Genes’ template showing the SpellExpression Score.

Regulation of serum-induced lipid accumulation in human monocyte-derived macrophages by interferon-γ. Correlations with apolipoprotein E production, lipoprotein.

Figure 2. Temperature-entropy diagram and the flow resistances of the power plant model of Figure 1. From: Thermodynamic optimization of a triple-shaft.

Figure 4. (A) A schematic representation from constructs that include modifications in Flag-TDP-12xQ/N. TDP-12xQ/N F4/L (F147, 149, 229, 231/L); TDP-12xQ/N.

Fig. 1. Visual representation of [14C]2,4-D translocation in susceptible (A–E), resistant R1 (F), and resistant R2 (G) wild radish seedlings.

Fig. 1. RUbioSeq pipelines for exome variant detection and BS-Seq analyses. Dark gray boxes correspond to the main steps of the pipelines. Light gray boxes.

Figure 1. The flow chart illustrates the construction process of anti-CRISPRdb, and the information that users can obtain from anti-CRISPRdb. From: Anti-CRISPRdb:

Figure 1. Cdc48 is cotranscriptionally recruited on active genes

Volume 14, Issue 6, Pages (December 2011)

Volume 14, Issue 4, Pages (October 2011)

Volume 22, Issue 8, Pages (February 2018)

Volume 4, Issue 1, Pages (January 2003)

Volume 20, Issue 10, Pages (September 2017)

Volume 137, Issue 3, Pages e4 (September 2009)

Figure 1. PNUTS-PP1 suppresses ATR signaling

Volume 19, Issue 4, Pages (April 2011)

Volume 10, Issue 4, Pages (October 2009)

Figure 1 The major structure of kisspeptins in humans, the peptides encoded by theKISS1gene. All kisspeptins are the products generated by the cleavage.

Volume 12, Issue 3, Pages (September 2010)

Volume 18, Issue 13, Pages (March 2017)

Figure 1. A CRISPR/Cas9 synthetic lethal screen with PRMT5 inhibitor EPZ in H2171 cell line. (A) A pie chart ... Figure 1. A CRISPR/Cas9 synthetic.

Figure 1. A novel image analysis tool to monitor epigenetic changes in spatiotemporal distribution of chromatin in live ... Figure 1. A novel image analysis.

Figure 7. Primary cells from prostate tumours are more sensitive to ML than adjacent non-cancerous cells from the ... Figure 7. Primary cells from.

Figure 6. HU sensitivity is due to the failure to process multiple consecutive ribonucleotides. 10-fold serial ... Figure 6. HU sensitivity is due to the.

Figure 1. BRCA1-associated R-Loop accumulation at a non-coding region upstream of ESR1 locus. (A) Alignment of DRIP-seq ... Figure 1. BRCA1-associated.

Figure 1. Designing a cell-specific Cas-ON switch based on miRNA-regulated anti-CRISPR genes. (A) Schematic of the ... Figure 1. Designing a cell-specific.

Volume 9, Issue 5, Pages (May 2009)

Figure 1 KCTD16 antibodies are associated with an underlying tumour

Volume 16, Issue 4, Pages (October 2012)

GRM7 Regulates Embryonic Neurogenesis via CREB and YAP

Figure 1. RSPO3 expression is upregulated in bladder cancer

Figure 1. LOC is highly expressed in NPC and predicts unfavorable prognosis. (A) Differential gene expression ... Figure 1. LOC is highly expressed.

Fig. 2 Case 2. Levels of serum creatinine and anti-GBM antibodies before and during treatment with cyclophosphamide, ... Fig. 2 Case 2. Levels of serum.

Volume 8, Issue 5, Pages (November 2008)

Figure 1. EBOV VP35 has NTP-binding and NTPase activities

Fig. 1. iS-CellR pipeline overview

Figure 1. Schematic diagram of solar energy and coal-fired power generation system. Unless provided in the caption above, the following copyright applies.

Hong Du, Mark Levine, Chandrashekar Ganesa, David P. Witte, Edward S

Volume 16, Issue 4, Pages (October 2012)

Figure 1. Accumulation kinetics of TC-NER factors reveal a CSA independent UVSSA recruitment. (A) Representative images ... Figure 1. Accumulation kinetics.

Figure 1. Workflow of the analysis to estimate the number of true human miRNAs. Samples containing NGS data were ... Figure 1. Workflow of the analysis.

Figure 1 Correlation between en face Oil-Red O staining and aortic root lesion size vs. plasma cholesterol and ... Figure 1 Correlation between en face.

Figure 1. 3C analysis of HEM3, BLM10, and SEN1 genes in rpb4Δ and isogenic wild type cells. (A) Schematic ... Figure 1. 3C analysis of HEM3, BLM10, and.

Figure 1. CSB does not affect the recruitment of OGG1 to oxidative DNA damage. (A) Representative stills of time-lapse ... Figure 1. CSB does not affect.

Ceramide Is Metabolized to Acylceramide and Stored in Lipid Droplets

Figure 1 The workflow of CAR development from a hybridoma

FIGURE 1 Changes in lipids and lipoproteins after consuming a Med-Red or Med-Control diet for 5 wk. Results are ... FIGURE 1 Changes in lipids and lipoproteins.

Figure 5. The endonucleolytic product from PfuPCNA/MR activity is displaced from dsDNA. Results from real-time ... Figure 5. The endonucleolytic product.

Presentation transcript:

Figure 3. Reduced fat absorption of Arfrp1<sup>vil−/−</sup> mice. (A) A fat tolerance test was performed in 5 h fasted Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice, and plasma triacylglycerol concentrations were detected at the indicated time points after the inhibition of lipoprotein catabolism by i.v. injection of Triton WR-1339. (B) FPLC profiles of plasma samples of Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice (n = 6) that received an oil bolus plus Triton WR-1339. Triacylglycerol concentrations (mmol/l) were detected in the different fractions, chylomicron/VLDL (fractions 4–7), IDL (fractions 8,9), LDL (fractions 10–16) and HDL (fractions 17–24). From: The GTPase ARFRP1 controls the lipidation of chylomicrons in the Golgi of the intestinal epithelium Hum Mol Genet. 2012;21(14):3128-3142. doi:10.1093/hmg/dds140 Hum Mol Genet | © The Author 2012. Published by Oxford University Press.This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Figure 2. Lethality and impaired triacylglycerol absorption of Arfrp1<sup>vil−/−</sup> mice. (A) Survival curves of Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice that were fed with either a standard diet, fat-depleted or carbohydrate-free (carb-free) diet over a time period of 35 days. (B) Triacylglycerol concentrations during fat tolerance tests performed in 5-week-old Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice. Values are means of eight mice ± SEM (*P< 0.05). (C) Impaired lipid release of Caco-2 cells after the down-regulation of Arfrp1 expression. Caco-2 cells were transfected with scrambled or Arfrp1-specific siRNA and harvested 4 and 8 days after transfection for western blot analysis with the anti-ARFRP1 antiserum (upper panel). Caco-2 cells were incubated with <sup>14</sup>C-labeled palmitate for 24 h, and radioactivity was determined in the basolateral medium reflecting the release (lower right panel) and in the lysates of the cells which indicates the retention (lower middle panel). The uptake was calculated as the sum of radioactivity in the cell lysates and the basolateral medium (lower left panel). (D) Time course of impaired lipid release from Arfrp1 knockdown Caco-2 cells. Cells were treated with <sup>14</sup>C-labeled palmitate in the apical medium, and lipid transport was measured at the indicated time points over the next 24 h. (E) Caco-2 cells transfected with scrambled or Arfrp1 siRNA were treated with 4 mm oleic acid for 24 h, and triacylglycerol levels in the cells (left panel) and the basal media (right panel) were measured. Values represent the mean ± SEM from three independent experiments (*P< 0.05). From: The GTPase ARFRP1 controls the lipidation of chylomicrons in the Golgi of the intestinal epithelium Hum Mol Genet. 2012;21(14):3128-3142. doi:10.1093/hmg/dds140 Hum Mol Genet | © The Author 2012. Published by Oxford University Press.This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Figure 1. Growth retardation of Arfrp1<sup>vil−/−</sup> mice. (A) Photographs of 3- and 28-day-old Arfrp1<sup>flox/flox</sup> (+/+) and Arfrp1<sup>vil−/−</sup> (−/−) mice. Body weights of Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice at the age of 3–28 days (n= 10–12). (B) Fat mass (left panel) and lean mass (right panel) of Arfrp1<sup>flox/flox</sup> (n= 26) and Arfrp1<sup>vil−/−</sup> mice (n= 10) at the age of 28 days. Values are means of 10–26 mice ± SEM (**P< 0.01, ***P< 0.001). From: The GTPase ARFRP1 controls the lipidation of chylomicrons in the Golgi of the intestinal epithelium Hum Mol Genet. 2012;21(14):3128-3142. doi:10.1093/hmg/dds140 Hum Mol Genet | © The Author 2012. Published by Oxford University Press.This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Figure 4. Impaired assembly of ApoA-I to chylomicrons in the intestinal epithelium of Arfrp1<sup>vil−/−</sup> mice. (A) Plasma of 16 h fasted Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice (0 h) or of mice 4 h after receiving an oil bolus was analyzed by western blotting with the indicated antibodies. (B) Quantification of the levels of indicated Apo in the plasma of fasted and oil-treated Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice (n= 10–11). (C) Triacylglycerol concentrations and levels of the indicated Apo in the chylomicron fractions of plasma from Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice that had received an oil bolus plus Triton WR-1339. (D) Immunohistochemical detection of indicated Apo in the intestinal section of Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice that were fasted and sacrificed 2 h after the olive oil bolus. Controls had free access to their regular standard diet. (E) Ultrastructural analysis of epithelial cells of Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice. Pictures show representative Golgi structures of control and knockout epithelial cells. The arrows depict premature chylomicrons that were rarely visible in the Golgi lumen of control cells but accumulated in that of Arfrp1<sup>vil−/−</sup> cells (G: Golgi apparatus; N: nucleus; CM: chylomicrons). From: The GTPase ARFRP1 controls the lipidation of chylomicrons in the Golgi of the intestinal epithelium Hum Mol Genet. 2012;21(14):3128-3142. doi:10.1093/hmg/dds140 Hum Mol Genet | © The Author 2012. Published by Oxford University Press.This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Figure 4. Impaired assembly of ApoA-I to chylomicrons in the intestinal epithelium of Arfrp1<sup>vil−/−</sup> mice. (A) Plasma of 16 h fasted Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice (0 h) or of mice 4 h after receiving an oil bolus was analyzed by western blotting with the indicated antibodies. (B) Quantification of the levels of indicated Apo in the plasma of fasted and oil-treated Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice (n= 10–11). (C) Triacylglycerol concentrations and levels of the indicated Apo in the chylomicron fractions of plasma from Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice that had received an oil bolus plus Triton WR-1339. (D) Immunohistochemical detection of indicated Apo in the intestinal section of Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice that were fasted and sacrificed 2 h after the olive oil bolus. Controls had free access to their regular standard diet. (E) Ultrastructural analysis of epithelial cells of Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice. Pictures show representative Golgi structures of control and knockout epithelial cells. The arrows depict premature chylomicrons that were rarely visible in the Golgi lumen of control cells but accumulated in that of Arfrp1<sup>vil−/−</sup> cells (G: Golgi apparatus; N: nucleus; CM: chylomicrons). From: The GTPase ARFRP1 controls the lipidation of chylomicrons in the Golgi of the intestinal epithelium Hum Mol Genet. 2012;21(14):3128-3142. doi:10.1093/hmg/dds140 Hum Mol Genet | © The Author 2012. Published by Oxford University Press.This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Figure 4. Impaired assembly of ApoA-I to chylomicrons in the intestinal epithelium of Arfrp1<sup>vil−/−</sup> mice. (A) Plasma of 16 h fasted Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice (0 h) or of mice 4 h after receiving an oil bolus was analyzed by western blotting with the indicated antibodies. (B) Quantification of the levels of indicated Apo in the plasma of fasted and oil-treated Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice (n= 10–11). (C) Triacylglycerol concentrations and levels of the indicated Apo in the chylomicron fractions of plasma from Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice that had received an oil bolus plus Triton WR-1339. (D) Immunohistochemical detection of indicated Apo in the intestinal section of Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice that were fasted and sacrificed 2 h after the olive oil bolus. Controls had free access to their regular standard diet. (E) Ultrastructural analysis of epithelial cells of Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice. Pictures show representative Golgi structures of control and knockout epithelial cells. The arrows depict premature chylomicrons that were rarely visible in the Golgi lumen of control cells but accumulated in that of Arfrp1<sup>vil−/−</sup> cells (G: Golgi apparatus; N: nucleus; CM: chylomicrons). From: The GTPase ARFRP1 controls the lipidation of chylomicrons in the Golgi of the intestinal epithelium Hum Mol Genet. 2012;21(14):3128-3142. doi:10.1093/hmg/dds140 Hum Mol Genet | © The Author 2012. Published by Oxford University Press.This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Figure 5. Reduced release of ApoA-I after the inhibition of Arfrp1 expression by siRNA in Caco-2 cells. (A) Scrambled and Arfrp1-siRNA transfected cells were treated with or without oleic acid for 24 h and indicated proteins detected in the basolateral medium or cell lysate by western blotting. (B) Quantification of levels of indicated Apo released into the basolateral medium of control (scrambled) and Arfrp1 knockdown (siArfrp1) Caco-2 cells (n= 8). (C) Normal lipid release from Caco-2 cells after the down-regulation of ApoA-I expression. Caco-2 cells were transfected with scrambled or ApoA1 siRNA and differentiated as described in Materials and methods. Cells were treated with 4 mm oleic acid for 24 h. The ApoA-I expression levels in the cell and in the basal media were determined by western blotting (top panel). Triacylglycerol levels were determined in the cells (bottom left panel) and the basal media (bottom right panel). Values represent the mean ± SEM. From: The GTPase ARFRP1 controls the lipidation of chylomicrons in the Golgi of the intestinal epithelium Hum Mol Genet. 2012;21(14):3128-3142. doi:10.1093/hmg/dds140 Hum Mol Genet | © The Author 2012. Published by Oxford University Press.This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Figure 6. Co-localization of Rab2 with ApoA-I and its accumulation at Golgi membranes of intestinal Arfrp1<sup>vil−/−</sup> cells. (A and B) Immunohistochemical detection of Rab2 (left panels), ApoA-I (middle panels) and the merged picture (right panels) in sections of the small intestine of 4-week-old Arfrp1<sup>flox/flox</sup> and Arfrp1<sup>vil−/−</sup> mice that had free access to their diet (A) or which received an oil bolus after a 16-h fasting period (B). (C) Color scatter plots of pictures from intestinal epithelial sections of mice after the oil application (upper panel) and Mander's co-localization coefficient (lower panel) for channel 1 (M1; ApoA-I) and channel 2 (M2, Rab2). (D) Co-staining of ARFRP1 and Golgin-245 (upper panels), ApoA-I and Golgin-245 (middle panels) and Rab2 and ApoA-I (lower panels) in Caco-2 cells. (E) Co-localization of Rab2 with ApoA-1 and ARFRP1 in Golgi subcellular fractions. Subcellular fractions were isolated from differentiated Caco-2 cells with OptiPrep™ as described in Materials and methods. Indicated proteins in the fractions were concentrated and analyzed by western blotting. From: The GTPase ARFRP1 controls the lipidation of chylomicrons in the Golgi of the intestinal epithelium Hum Mol Genet. 2012;21(14):3128-3142. doi:10.1093/hmg/dds140 Hum Mol Genet | © The Author 2012. Published by Oxford University Press.This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Figure 7. Impaired triglyceride release from Caco-2 cells after the suppression of Arl1 (A), Golgin-245 (B) and Rab2 (C) expression. Caco-2 cells were transfected with scrambled or the indicated siRNAs and harvested 8 days after transfection for western blotting with the different antisera (top panels). Caco-2 cells were incubated with 4 mm oleic acid for 24 h, and triacylglycerol levels were measured in the cells (left panels) and the basal media (right panels). From: The GTPase ARFRP1 controls the lipidation of chylomicrons in the Golgi of the intestinal epithelium Hum Mol Genet. 2012;21(14):3128-3142. doi:10.1093/hmg/dds140 Hum Mol Genet | © The Author 2012. Published by Oxford University Press.This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Figure 8. Model of the role of the ARFRP1-ARL1-Golgin-Rab2 cascade for chylomicron maturation. (A) ARFRP1 is necessary to recruit ARL1 to the Golgi, ARL1 binds to the GRIP domain of the scaffolding protein Golgin-245 which binds Rab2 via the coiled-coil domain. (B) Chylomicron formation in the ER and the Golgi. In the ER, monoacylglycerol acyltransferase (MGAT) and diacylglycerol acyltransferase (DGAT) catalyze the synthesis of triacylglycerol (TAG) which is incorporated into ApoB48-containing pre-chylomicrons. Subsequently, ApoA-IV binds to the pre-chylomicrons which are then released to the cis-Golgi and further lipidated in the Golgi. ApoA-I is synthesized in the ER and transported to the Golgi where it is attached to the chylomicrons. ApoA-I loaded chylomicrons are then transported through the Golgi, released on the trans-site and finally secreted into the lymph. We propose that the ARFRP1-ARL1-Golgin-Rab2 cascade is needed for an appropriate chylomicron assembly of ApoA-I, its transport through and lipidation within the Golgi. From: The GTPase ARFRP1 controls the lipidation of chylomicrons in the Golgi of the intestinal epithelium Hum Mol Genet. 2012;21(14):3128-3142. doi:10.1093/hmg/dds140 Hum Mol Genet | © The Author 2012. Published by Oxford University Press.This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.