Characterisation of <i>Ptprj-as1.</i>

<p>A–B: <i>Ptprj-as1</i> maps to the reverse strand within the boundaries of the murine <i>Ptprj</i> gene. Comparison of the mouse Ptprj (A) and human PTPRJ (B) loci. Protein coding transcript isoforms of Ptprj/PTPRJ are shown in red and long noncoding transcripts are shown in blue. Arrows indicate the direction of transcription. The human microRNA miR-3161 is shown in green. Position of PCR primers used for qRT-PCR for mouse Ptprj-as1 are indicated. C-D: Mapping (C) and expression (D) of a splice variant of murine <i>Ptprj-as1</i> in brain, kidney and testis. E: Predicted secondary structure of <i>Ptprj-as1</i> splice variant.</p

Expression of <i>Ptprj-as1</i> in murine tissues and in response to TRL ligands.

<p>A: Expression of <i>Ptprj-as1</i> in murine tissues. B, C: <i>Ptprj</i> and <i>Ptprj-as1</i> mRNA expression in BMMs in response to LPS (B) or Pam3Cys (C). mRNA expression was quantified by qRT-PCR and expressed as fold change compared with untreated (0h). Plots represent mean fold change +/− SD; n = 3. Significance values were determined by one-way analysis of variance (ANOVA). *denotes p<0.05; **denotes p<0.005; n = 3. *denotes p<0.05; **denotes p<0.005; n = 3.</p

Regulation of <i>Ptprj</i> expression in mouse macrophages by proinflammatory stimuli.

<p>A–C: Regulation of <i>Ptprj</i> expression by CSF-1 and LPS in mouse bone marrow-derived macrophages (BMMs). BMMs were maintained overnight in the presence or absence of CSF-1 (1×10⁴ U/mL) before treatment with LPS (10 ng/mL) (A, B). RAW 264.7 cells were maintained overnight in the absence of CSF-1 before treatment with LPS (10 ng/mL) (C). <i>Ptprj</i> (A, C) and <i>c-fms</i> (B) expression profiles were assessed by quantitative real-time PCR. Profiles are representative of two independent experiments. D: Regulation of <i>Ptprj</i> expression by CSF-1 and LPS in mouse thioglycollate-elicited peritoneal macrophages (TEPMs). TEPMs were maintained overnight in the presence or absence of CSF-1 (1×10⁴ U/mL) before treatment with LPS (10 ng/mL). <i>Ptprj</i> expression profile was assessed by quantitative real-time PCR. E: IFNγ treatment of bone marrow derived macrophages suppresses the LPS mediated induction of <i>ptprj</i>. BMMs were maintained overnight in the presence of CSF-1 (1×10⁴ U/mL) and presence or absence of IFNγ (500 pg/mL) before treatment with LPS (10 ng/mL). RNA was extracted at each time point and used for the synthesis of cDNA. <i>Ptprj</i> expression profile was assessed by quantitative real-time PCR. Datapoints (+/− SD) represent the average of triplicate samples each from triplicate independent experiments. Significance values were determined by one-way analysis of variance (ANOVA). *denotes p<0.05; **denotes p<0.005; n = 3. F: Regulation of <i>PTPRJ</i> protein in response to LPS, CpG DNA and CSF-1. BMMs were maintained overnight in the presence or absence of CSF-1 (1×10⁴ U/mL) before treatment with LPS (10 ng/mL) [top panel] or CpG DNA (0.1 µM) [bottom panel]. Protein lysates were separated by SDS-PAGE, transferred to PVDF membranes and immunoblotted for PTPRJ. The membrane was then stripped, and reprobed for total Akt as a loading control. Profiles are representative of two independent experiments.</p

Ptprj mRNA expression in murine tissues.

<p>(A). qPCR of <i>Ptprj</i> from RNA extracted from mouse tissues. (B) qPCR of <i>Ptprj</i> from RNA from pre-B lymphoid cell line WEHI-231, osteoclast-like cell line (RAW 264.7, C4), TEPM, macrophage-like cell line (RAW 264.7), BMM, myeloid cell line M1 and fibroblasts (NIH3T3 and mouse embryonic). (C). Immunohistochemistry of cell-specific expression of PTPRJ in mouse spleen sections. Sections were immunostained for CD148 (A1, B1) or F4/80 (A2, B2) and with CD148 (C1) and F4/80 (C2) isotype control antibodies. All sections were counterstained with haematoxylin. RP, red pulp; WP, white pulp. Original magnification: x100 (A), x200 (B, C). Bar, 100µm.</p

<i>Ptprj</i> expression in response to LPS in human mononuclear phagocytic cells.

<p>THP-1 cells were maintained for 24 hours in the presence or absence of PMA (10⁻⁷ M) to induce differentiation, before treatment with LPS (10 ng/mL) (A, B). Human dendritic cells were treated with LPS (10 ng/mL) over a time course (C, D). <i>Ptprj</i> (A, C) and <i>c-fms</i> (B, D) expression profiles were assessed by quantitative real-time PCR. Datapoints (+/− SD) represent the average of triplicate samples. Significance values were determined by one-way analysis of variance (ANOVA). *denotes p<0.05; **denotes p<0.005; n = 3. *denotes p<0.05; **denotes p<0.005; n = 3.</p

Expression analysis of G Protein-Coupled Receptors in mouse macrophages-0

Of 91 murine cell types and tissues. Data points show normalised values and similar cell types are grouped according to bar colour; blue indicates primary macrophage cell types, purple indicates bone-related cell types, red indicates other immune cell types, green indicates stem cell populations, orange indicates whole tissue samples, yellow indicates neuronal and retinal cell types and pink indicates cell lines. Additional file gives details of the 91 cell types and tissues profiled.<p><b>Copyright information:</b></p><p>Taken from "Expression analysis of G Protein-Coupled Receptors in mouse macrophages"</p><p>http://www.immunome-research.com/content/4/1/5</p><p>Immunome Research 2008;4():5-5.</p><p>Published online 29 Apr 2008</p><p>PMCID:PMC2394514.</p><p></p

Expression analysis of G Protein-Coupled Receptors in mouse macrophages-2

over a timecourse of 0, 2, 6, and 24 h, and 0, 1 and 7 h, respectively. Data points show gene expression relative to untreated control for each cell population (0 h).<p><b>Copyright information:</b></p><p>Taken from "Expression analysis of G Protein-Coupled Receptors in mouse macrophages"</p><p>http://www.immunome-research.com/content/4/1/5</p><p>Immunome Research 2008;4():5-5.</p><p>Published online 29 Apr 2008</p><p>PMCID:PMC2394514.</p><p></p

Expression analysis of G Protein-Coupled Receptors in mouse macrophages-1

Of 91 murine cell types and tissues. Data points show normalised values and similar cell types are grouped according to bar colour; blue indicates primary macrophage cell types, purple indicates bone-related cell types, red indicates other immune cell types, green indicates stem cell populations, orange indicates whole tissue samples, yellow indicates neuronal and retinal cell types and pink indicates cell lines. Additional file gives details of the 91 cell types and tissues profiled.<p><b>Copyright information:</b></p><p>Taken from "Expression analysis of G Protein-Coupled Receptors in mouse macrophages"</p><p>http://www.immunome-research.com/content/4/1/5</p><p>Immunome Research 2008;4():5-5.</p><p>Published online 29 Apr 2008</p><p>PMCID:PMC2394514.</p><p></p

Slfn4 over-expression caused splenomegaly.

<p>(A) Macroscopic appearance of spleens from <i>Slfn4</i> over-expressing mice (right) and from MacBlue littermate controls (left). (B) Organ weights are expressed as percentage of body weight. Data are combined from four independent experiments and are displayed as mean + SEM.</p

Putative regulatory elements within the <i>Slfn4</i> promoter.

<p>The <i>Slfn4</i> proximal promoter is a TATA-containing promoter with putative binding sites for STAT1, IRF family members, PU.1 and AP1. The TSS, designated +1, is marked with an arrow.</p