rtn4 Search Results


90
Sino Biological rtn4 sino biological
Figure 7. METTL7B-interacting proteins are enriched in the ER and LDs (A) Venn diagram of high-confidence METTL7B-interacting proteins revealed by HaloTag and BioID. (B) KEGG enrichment of METTL7B interacting proteins from the intersection of HaloTag and BioID. (C) Interaction network with proteins in KEGG protein processing in the ER pathway (gray) and AD pathway (orange). METTL7B interactors are shown as filled circles. (D and E) Immunoblot confirmation of top interacting candidates. The molecular weight of the <t>RTN4-immunoreactive</t> band is consistent with a known proteolytic fragment of RTN4A or RTN4B (Kim et al., 2003; Sekine et al., 2020). (F) SAM methyltransferase activity assay showing increased reactivity in the presence of METTL7B. The p values were calculated by unpaired two-tailed Stu- dent’s t test; n = 3. (G and H) Immunoanalysis of METTL7B translocation. An increased fatty acid (FA) load leads to a shift of METTL7B from the ER to lipid droplets (LDs), whereas high-confidence interactors remain unaffected. Blocking translation of new proteins with cycloheximide (Cyhx) suggests a complete shift of METTL7B. Scale bar, 10 mm. CY, cytosol; SO, sedimented organelle (containing the ER). All data are mean ± SEM. ****p < 0.0001, ***p < 0.001. See also Figures S6 and S7 and Table S4.
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Cusabio elisa kits
Figure 7. METTL7B-interacting proteins are enriched in the ER and LDs (A) Venn diagram of high-confidence METTL7B-interacting proteins revealed by HaloTag and BioID. (B) KEGG enrichment of METTL7B interacting proteins from the intersection of HaloTag and BioID. (C) Interaction network with proteins in KEGG protein processing in the ER pathway (gray) and AD pathway (orange). METTL7B interactors are shown as filled circles. (D and E) Immunoblot confirmation of top interacting candidates. The molecular weight of the <t>RTN4-immunoreactive</t> band is consistent with a known proteolytic fragment of RTN4A or RTN4B (Kim et al., 2003; Sekine et al., 2020). (F) SAM methyltransferase activity assay showing increased reactivity in the presence of METTL7B. The p values were calculated by unpaired two-tailed Stu- dent’s t test; n = 3. (G and H) Immunoanalysis of METTL7B translocation. An increased fatty acid (FA) load leads to a shift of METTL7B from the ER to lipid droplets (LDs), whereas high-confidence interactors remain unaffected. Blocking translation of new proteins with cycloheximide (Cyhx) suggests a complete shift of METTL7B. Scale bar, 10 mm. CY, cytosol; SO, sedimented organelle (containing the ER). All data are mean ± SEM. ****p < 0.0001, ***p < 0.001. See also Figures S6 and S7 and Table S4.
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OriGene prk5 c flag
Figure 7. METTL7B-interacting proteins are enriched in the ER and LDs (A) Venn diagram of high-confidence METTL7B-interacting proteins revealed by HaloTag and BioID. (B) KEGG enrichment of METTL7B interacting proteins from the intersection of HaloTag and BioID. (C) Interaction network with proteins in KEGG protein processing in the ER pathway (gray) and AD pathway (orange). METTL7B interactors are shown as filled circles. (D and E) Immunoblot confirmation of top interacting candidates. The molecular weight of the <t>RTN4-immunoreactive</t> band is consistent with a known proteolytic fragment of RTN4A or RTN4B (Kim et al., 2003; Sekine et al., 2020). (F) SAM methyltransferase activity assay showing increased reactivity in the presence of METTL7B. The p values were calculated by unpaired two-tailed Stu- dent’s t test; n = 3. (G and H) Immunoanalysis of METTL7B translocation. An increased fatty acid (FA) load leads to a shift of METTL7B from the ER to lipid droplets (LDs), whereas high-confidence interactors remain unaffected. Blocking translation of new proteins with cycloheximide (Cyhx) suggests a complete shift of METTL7B. Scale bar, 10 mm. CY, cytosol; SO, sedimented organelle (containing the ER). All data are mean ± SEM. ****p < 0.0001, ***p < 0.001. See also Figures S6 and S7 and Table S4.
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Proteintech rabbit anti rtn4
Figure 7. METTL7B-interacting proteins are enriched in the ER and LDs (A) Venn diagram of high-confidence METTL7B-interacting proteins revealed by HaloTag and BioID. (B) KEGG enrichment of METTL7B interacting proteins from the intersection of HaloTag and BioID. (C) Interaction network with proteins in KEGG protein processing in the ER pathway (gray) and AD pathway (orange). METTL7B interactors are shown as filled circles. (D and E) Immunoblot confirmation of top interacting candidates. The molecular weight of the <t>RTN4-immunoreactive</t> band is consistent with a known proteolytic fragment of RTN4A or RTN4B (Kim et al., 2003; Sekine et al., 2020). (F) SAM methyltransferase activity assay showing increased reactivity in the presence of METTL7B. The p values were calculated by unpaired two-tailed Stu- dent’s t test; n = 3. (G and H) Immunoanalysis of METTL7B translocation. An increased fatty acid (FA) load leads to a shift of METTL7B from the ER to lipid droplets (LDs), whereas high-confidence interactors remain unaffected. Blocking translation of new proteins with cycloheximide (Cyhx) suggests a complete shift of METTL7B. Scale bar, 10 mm. CY, cytosol; SO, sedimented organelle (containing the ER). All data are mean ± SEM. ****p < 0.0001, ***p < 0.001. See also Figures S6 and S7 and Table S4.
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Thermo Fisher gene exp rtn4 mm00445861 m1
Figure 7. METTL7B-interacting proteins are enriched in the ER and LDs (A) Venn diagram of high-confidence METTL7B-interacting proteins revealed by HaloTag and BioID. (B) KEGG enrichment of METTL7B interacting proteins from the intersection of HaloTag and BioID. (C) Interaction network with proteins in KEGG protein processing in the ER pathway (gray) and AD pathway (orange). METTL7B interactors are shown as filled circles. (D and E) Immunoblot confirmation of top interacting candidates. The molecular weight of the <t>RTN4-immunoreactive</t> band is consistent with a known proteolytic fragment of RTN4A or RTN4B (Kim et al., 2003; Sekine et al., 2020). (F) SAM methyltransferase activity assay showing increased reactivity in the presence of METTL7B. The p values were calculated by unpaired two-tailed Stu- dent’s t test; n = 3. (G and H) Immunoanalysis of METTL7B translocation. An increased fatty acid (FA) load leads to a shift of METTL7B from the ER to lipid droplets (LDs), whereas high-confidence interactors remain unaffected. Blocking translation of new proteins with cycloheximide (Cyhx) suggests a complete shift of METTL7B. Scale bar, 10 mm. CY, cytosol; SO, sedimented organelle (containing the ER). All data are mean ± SEM. ****p < 0.0001, ***p < 0.001. See also Figures S6 and S7 and Table S4.
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Addgene inc rtn4
Figure 7. METTL7B-interacting proteins are enriched in the ER and LDs (A) Venn diagram of high-confidence METTL7B-interacting proteins revealed by HaloTag and BioID. (B) KEGG enrichment of METTL7B interacting proteins from the intersection of HaloTag and BioID. (C) Interaction network with proteins in KEGG protein processing in the ER pathway (gray) and AD pathway (orange). METTL7B interactors are shown as filled circles. (D and E) Immunoblot confirmation of top interacting candidates. The molecular weight of the <t>RTN4-immunoreactive</t> band is consistent with a known proteolytic fragment of RTN4A or RTN4B (Kim et al., 2003; Sekine et al., 2020). (F) SAM methyltransferase activity assay showing increased reactivity in the presence of METTL7B. The p values were calculated by unpaired two-tailed Stu- dent’s t test; n = 3. (G and H) Immunoanalysis of METTL7B translocation. An increased fatty acid (FA) load leads to a shift of METTL7B from the ER to lipid droplets (LDs), whereas high-confidence interactors remain unaffected. Blocking translation of new proteins with cycloheximide (Cyhx) suggests a complete shift of METTL7B. Scale bar, 10 mm. CY, cytosol; SO, sedimented organelle (containing the ER). All data are mean ± SEM. ****p < 0.0001, ***p < 0.001. See also Figures S6 and S7 and Table S4.
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Proteintech rabbit anti rtn4 polyclonal antibody
BMM (treated with siRNA to either CLIMP-63 or <t>RTN4</t> or treated with control siRNA, Ctr) were infected with L. donovani or L. amazonensis metacyclic promastigotes and at various time points post-phagocytosis parasite replication and PV size were assessed. (A) Quantification of L. donovani parasite burden in CLIMP-63 depleted BMM at 6, 24, 48, and 72 h post-infection. (B) Quantification of L. amazonensis parasite burden in CLIMP-63 depleted BMM at 6, 24, 48, and 72 h post-infection. (C) Quantification of PV size in CLIMP-63-depleted BMM infected with L. amazonensis at 48 and 72 h post-phagocytosis. (D) Quantification of L. donovani parasite burden in RTN4-depleted BMM at 6, 24, 48, and 72 h post-infection. (E) Quantification of L. amazonensis parasite burden in RTN4-depleted BMM at 6, 24, 48, and 72 h post-infection. (F) Quantification of PV size in RTN4-depleted BMM infected with L. amazonensis at 48 and 72 h post-phagocytosis. Data in (A, B, D, E) are presented as the means ± SEM of values of one representative experiment of three independent experiments. Data in (C, F) are presented as a violin plot with means ± standard deviations (SD) of values from three independent experiments for a total of 450 PVs. Statistics were calculated using one-way analyses of variance (ANOVA) with Sidak’s multiple comparison test with * P ≤ 0.05, *** P ≤ 0.001 and **** P ≤ 0.0001 significance. Blots showing the efficacy the siRNA-mediated CLIMP-63 and RTN4 knockdowns are shown in S3 Fig and S4 Fig, respectively.
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Boster Bio rtn4
BMM (treated with siRNA to either CLIMP-63 or <t>RTN4</t> or treated with control siRNA, Ctr) were infected with L. donovani or L. amazonensis metacyclic promastigotes and at various time points post-phagocytosis parasite replication and PV size were assessed. (A) Quantification of L. donovani parasite burden in CLIMP-63 depleted BMM at 6, 24, 48, and 72 h post-infection. (B) Quantification of L. amazonensis parasite burden in CLIMP-63 depleted BMM at 6, 24, 48, and 72 h post-infection. (C) Quantification of PV size in CLIMP-63-depleted BMM infected with L. amazonensis at 48 and 72 h post-phagocytosis. (D) Quantification of L. donovani parasite burden in RTN4-depleted BMM at 6, 24, 48, and 72 h post-infection. (E) Quantification of L. amazonensis parasite burden in RTN4-depleted BMM at 6, 24, 48, and 72 h post-infection. (F) Quantification of PV size in RTN4-depleted BMM infected with L. amazonensis at 48 and 72 h post-phagocytosis. Data in (A, B, D, E) are presented as the means ± SEM of values of one representative experiment of three independent experiments. Data in (C, F) are presented as a violin plot with means ± standard deviations (SD) of values from three independent experiments for a total of 450 PVs. Statistics were calculated using one-way analyses of variance (ANOVA) with Sidak’s multiple comparison test with * P ≤ 0.05, *** P ≤ 0.001 and **** P ≤ 0.0001 significance. Blots showing the efficacy the siRNA-mediated CLIMP-63 and RTN4 knockdowns are shown in S3 Fig and S4 Fig, respectively.
Rtn4, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Boster Bio nogo a
BMM (treated with siRNA to either CLIMP-63 or <t>RTN4</t> or treated with control siRNA, Ctr) were infected with L. donovani or L. amazonensis metacyclic promastigotes and at various time points post-phagocytosis parasite replication and PV size were assessed. (A) Quantification of L. donovani parasite burden in CLIMP-63 depleted BMM at 6, 24, 48, and 72 h post-infection. (B) Quantification of L. amazonensis parasite burden in CLIMP-63 depleted BMM at 6, 24, 48, and 72 h post-infection. (C) Quantification of PV size in CLIMP-63-depleted BMM infected with L. amazonensis at 48 and 72 h post-phagocytosis. (D) Quantification of L. donovani parasite burden in RTN4-depleted BMM at 6, 24, 48, and 72 h post-infection. (E) Quantification of L. amazonensis parasite burden in RTN4-depleted BMM at 6, 24, 48, and 72 h post-infection. (F) Quantification of PV size in RTN4-depleted BMM infected with L. amazonensis at 48 and 72 h post-phagocytosis. Data in (A, B, D, E) are presented as the means ± SEM of values of one representative experiment of three independent experiments. Data in (C, F) are presented as a violin plot with means ± standard deviations (SD) of values from three independent experiments for a total of 450 PVs. Statistics were calculated using one-way analyses of variance (ANOVA) with Sidak’s multiple comparison test with * P ≤ 0.05, *** P ≤ 0.001 and **** P ≤ 0.0001 significance. Blots showing the efficacy the siRNA-mediated CLIMP-63 and RTN4 knockdowns are shown in S3 Fig and S4 Fig, respectively.
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Thermo Fisher snp rtn4 c 2128452 20
BMM (treated with siRNA to either CLIMP-63 or <t>RTN4</t> or treated with control siRNA, Ctr) were infected with L. donovani or L. amazonensis metacyclic promastigotes and at various time points post-phagocytosis parasite replication and PV size were assessed. (A) Quantification of L. donovani parasite burden in CLIMP-63 depleted BMM at 6, 24, 48, and 72 h post-infection. (B) Quantification of L. amazonensis parasite burden in CLIMP-63 depleted BMM at 6, 24, 48, and 72 h post-infection. (C) Quantification of PV size in CLIMP-63-depleted BMM infected with L. amazonensis at 48 and 72 h post-phagocytosis. (D) Quantification of L. donovani parasite burden in RTN4-depleted BMM at 6, 24, 48, and 72 h post-infection. (E) Quantification of L. amazonensis parasite burden in RTN4-depleted BMM at 6, 24, 48, and 72 h post-infection. (F) Quantification of PV size in RTN4-depleted BMM infected with L. amazonensis at 48 and 72 h post-phagocytosis. Data in (A, B, D, E) are presented as the means ± SEM of values of one representative experiment of three independent experiments. Data in (C, F) are presented as a violin plot with means ± standard deviations (SD) of values from three independent experiments for a total of 450 PVs. Statistics were calculated using one-way analyses of variance (ANOVA) with Sidak’s multiple comparison test with * P ≤ 0.05, *** P ≤ 0.001 and **** P ≤ 0.0001 significance. Blots showing the efficacy the siRNA-mediated CLIMP-63 and RTN4 knockdowns are shown in S3 Fig and S4 Fig, respectively.
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Aviva Systems anti reticulon 4
BMM (treated with siRNA to either CLIMP-63 or <t>RTN4</t> or treated with control siRNA, Ctr) were infected with L. donovani or L. amazonensis metacyclic promastigotes and at various time points post-phagocytosis parasite replication and PV size were assessed. (A) Quantification of L. donovani parasite burden in CLIMP-63 depleted BMM at 6, 24, 48, and 72 h post-infection. (B) Quantification of L. amazonensis parasite burden in CLIMP-63 depleted BMM at 6, 24, 48, and 72 h post-infection. (C) Quantification of PV size in CLIMP-63-depleted BMM infected with L. amazonensis at 48 and 72 h post-phagocytosis. (D) Quantification of L. donovani parasite burden in RTN4-depleted BMM at 6, 24, 48, and 72 h post-infection. (E) Quantification of L. amazonensis parasite burden in RTN4-depleted BMM at 6, 24, 48, and 72 h post-infection. (F) Quantification of PV size in RTN4-depleted BMM infected with L. amazonensis at 48 and 72 h post-phagocytosis. Data in (A, B, D, E) are presented as the means ± SEM of values of one representative experiment of three independent experiments. Data in (C, F) are presented as a violin plot with means ± standard deviations (SD) of values from three independent experiments for a total of 450 PVs. Statistics were calculated using one-way analyses of variance (ANOVA) with Sidak’s multiple comparison test with * P ≤ 0.05, *** P ≤ 0.001 and **** P ≤ 0.0001 significance. Blots showing the efficacy the siRNA-mediated CLIMP-63 and RTN4 knockdowns are shown in S3 Fig and S4 Fig, respectively.
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Thermo Fisher gene exp rtn4 rn00582903 m1
TaqMan gene expression assay information (RhoA/ROCK pathway)
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Image Search Results


Figure 7. METTL7B-interacting proteins are enriched in the ER and LDs (A) Venn diagram of high-confidence METTL7B-interacting proteins revealed by HaloTag and BioID. (B) KEGG enrichment of METTL7B interacting proteins from the intersection of HaloTag and BioID. (C) Interaction network with proteins in KEGG protein processing in the ER pathway (gray) and AD pathway (orange). METTL7B interactors are shown as filled circles. (D and E) Immunoblot confirmation of top interacting candidates. The molecular weight of the RTN4-immunoreactive band is consistent with a known proteolytic fragment of RTN4A or RTN4B (Kim et al., 2003; Sekine et al., 2020). (F) SAM methyltransferase activity assay showing increased reactivity in the presence of METTL7B. The p values were calculated by unpaired two-tailed Stu- dent’s t test; n = 3. (G and H) Immunoanalysis of METTL7B translocation. An increased fatty acid (FA) load leads to a shift of METTL7B from the ER to lipid droplets (LDs), whereas high-confidence interactors remain unaffected. Blocking translation of new proteins with cycloheximide (Cyhx) suggests a complete shift of METTL7B. Scale bar, 10 mm. CY, cytosol; SO, sedimented organelle (containing the ER). All data are mean ± SEM. ****p < 0.0001, ***p < 0.001. See also Figures S6 and S7 and Table S4.

Journal: Neuron

Article Title: Transcriptomic taxonomy and neurogenic trajectories of adult human, macaque, and pig hippocampal and entorhinal cells.

doi: 10.1016/j.neuron.2021.10.036

Figure Lengend Snippet: Figure 7. METTL7B-interacting proteins are enriched in the ER and LDs (A) Venn diagram of high-confidence METTL7B-interacting proteins revealed by HaloTag and BioID. (B) KEGG enrichment of METTL7B interacting proteins from the intersection of HaloTag and BioID. (C) Interaction network with proteins in KEGG protein processing in the ER pathway (gray) and AD pathway (orange). METTL7B interactors are shown as filled circles. (D and E) Immunoblot confirmation of top interacting candidates. The molecular weight of the RTN4-immunoreactive band is consistent with a known proteolytic fragment of RTN4A or RTN4B (Kim et al., 2003; Sekine et al., 2020). (F) SAM methyltransferase activity assay showing increased reactivity in the presence of METTL7B. The p values were calculated by unpaired two-tailed Stu- dent’s t test; n = 3. (G and H) Immunoanalysis of METTL7B translocation. An increased fatty acid (FA) load leads to a shift of METTL7B from the ER to lipid droplets (LDs), whereas high-confidence interactors remain unaffected. Blocking translation of new proteins with cycloheximide (Cyhx) suggests a complete shift of METTL7B. Scale bar, 10 mm. CY, cytosol; SO, sedimented organelle (containing the ER). All data are mean ± SEM. ****p < 0.0001, ***p < 0.001. See also Figures S6 and S7 and Table S4.

Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER METTL7B (24-244 aa) GenScript This paper RTN3 Antibodies-Online Cat#ABIN3111137 RTN4 Sino Biological Cat#13030-H09E Digoxigenin-UTP Roche Cat#11209256910 BsrGI New England BioLabs Cat#R0575L PacI New England BioLabs Cat#R0547L Klenow New England BioLabs Cat#M0210M Trypsin Gold, Mass Spectrometry Grade Promega Cat#V5280 PolyJet SignaGen Cat#SL100688 Protamine sulfate MP Biomedicals Cat#02194729 NBT/BCIP Stock Solution Roche Cat# 11681451001 Protector RNase Inhibitor Roche Cat#03335402001 cOmplete, EDTA-free Protease Inhibitor Cocktail Roche Cat#11836170001 Optiprep Axis-Shield Cat#1114542 Bovine Serum Albumin (BSA), Fraction V—Molecular Biology Grade Gemini Bio-Products Cat#700-106P Critical commercial assays Chromium Single Cell 3ʹGEM, Library & Gel Bead Kit v3 10x Genomics Cat#PN-1000075 TMRDirect (1:1000) Promega Cat#G2991 HaloTag Promega Cat#G6500 C18 TopTip PolyLC Cat#TT10C18.96 Chromium Single Cell B Chip Kit 10x Genomics Cat#PN-1000074 Chromium i7 Multiplex Kit (10x Genomics #PN-120262) 10x Genomics Cat#PN-120262 Deposited data Human adult hippocampus snRNA-seq This paper GSE186538 GRCh38 (Ensembl release 98) Ensembl, GENCODE https://www.gencodegenes.org/human/# Mmul10 UCSC, RefSeq https://hgdownload.soe.ucsc.edu/ goldenPath/rheMac10/bigZips/ susScr11 UCSC, RefSeq https://hgdownload.soe.ucsc.edu/ goldenPath/susScr11/bigZips/ PsychENCODE RNA-seq data Li et al., 2018 http://www.development. psychencode.org/ Developmental human brain exon array data Kang et al., 2011 https://hbatlas.org/ Human, chimpanzee and macaque RNA-seq data Zhu et al., 2018 https://evolution.psychencode.org/ Mammalian brain development RNA-seq data Cardoso-Moreira et al., 2019 https://apps.kaessmannlab.org/ evodevoapp/ Human fetal hippocampus scRNA-seq data Zhong et al., 2020 GSE131258 Mouse adult hippocampus scRNA-seq data Hochgerner et al., 2018 GSE95753 Human hippocampus DroNc-seq data Habib et al., 2017 https://singlecell.broadinstitute.org/ single_cell Axis-specific human hippocampus snRNA-seq data Ayhan et al., 2021 https://cells.ucsc.edu/?ds=human- hippo-axis snRNA-seq data of human Alzheimer’s disease brain middle temporal gyrus NCBI GEO GSE188545 (Continued on next page) Neuron 110, 452–469.e1–e14, February 2, 2022 e2

Techniques: Western Blot, Molecular Weight, Activity Assay, Two Tailed Test, Translocation Assay, Blocking Assay

BMM (treated with siRNA to either CLIMP-63 or RTN4 or treated with control siRNA, Ctr) were infected with L. donovani or L. amazonensis metacyclic promastigotes and at various time points post-phagocytosis parasite replication and PV size were assessed. (A) Quantification of L. donovani parasite burden in CLIMP-63 depleted BMM at 6, 24, 48, and 72 h post-infection. (B) Quantification of L. amazonensis parasite burden in CLIMP-63 depleted BMM at 6, 24, 48, and 72 h post-infection. (C) Quantification of PV size in CLIMP-63-depleted BMM infected with L. amazonensis at 48 and 72 h post-phagocytosis. (D) Quantification of L. donovani parasite burden in RTN4-depleted BMM at 6, 24, 48, and 72 h post-infection. (E) Quantification of L. amazonensis parasite burden in RTN4-depleted BMM at 6, 24, 48, and 72 h post-infection. (F) Quantification of PV size in RTN4-depleted BMM infected with L. amazonensis at 48 and 72 h post-phagocytosis. Data in (A, B, D, E) are presented as the means ± SEM of values of one representative experiment of three independent experiments. Data in (C, F) are presented as a violin plot with means ± standard deviations (SD) of values from three independent experiments for a total of 450 PVs. Statistics were calculated using one-way analyses of variance (ANOVA) with Sidak’s multiple comparison test with * P ≤ 0.05, *** P ≤ 0.001 and **** P ≤ 0.0001 significance. Blots showing the efficacy the siRNA-mediated CLIMP-63 and RTN4 knockdowns are shown in S3 Fig and S4 Fig, respectively.

Journal: bioRxiv

Article Title: Leishmania exploits the macrophage endoplasmic reticulum-shaping protein CLIMP-63 to modulate mitochondrial biogenesis and bioenergetics

doi: 10.64898/2026.03.19.712868

Figure Lengend Snippet: BMM (treated with siRNA to either CLIMP-63 or RTN4 or treated with control siRNA, Ctr) were infected with L. donovani or L. amazonensis metacyclic promastigotes and at various time points post-phagocytosis parasite replication and PV size were assessed. (A) Quantification of L. donovani parasite burden in CLIMP-63 depleted BMM at 6, 24, 48, and 72 h post-infection. (B) Quantification of L. amazonensis parasite burden in CLIMP-63 depleted BMM at 6, 24, 48, and 72 h post-infection. (C) Quantification of PV size in CLIMP-63-depleted BMM infected with L. amazonensis at 48 and 72 h post-phagocytosis. (D) Quantification of L. donovani parasite burden in RTN4-depleted BMM at 6, 24, 48, and 72 h post-infection. (E) Quantification of L. amazonensis parasite burden in RTN4-depleted BMM at 6, 24, 48, and 72 h post-infection. (F) Quantification of PV size in RTN4-depleted BMM infected with L. amazonensis at 48 and 72 h post-phagocytosis. Data in (A, B, D, E) are presented as the means ± SEM of values of one representative experiment of three independent experiments. Data in (C, F) are presented as a violin plot with means ± standard deviations (SD) of values from three independent experiments for a total of 450 PVs. Statistics were calculated using one-way analyses of variance (ANOVA) with Sidak’s multiple comparison test with * P ≤ 0.05, *** P ≤ 0.001 and **** P ≤ 0.0001 significance. Blots showing the efficacy the siRNA-mediated CLIMP-63 and RTN4 knockdowns are shown in S3 Fig and S4 Fig, respectively.

Article Snippet: The mouse anti-CLIMP-63 monoclonal antibody (sc-393544) was from Santa Cruz Biotechnology, the rabbit anti-RTN4 polyclonal antibody (ab186735) and the rat anti-BrdU (ab6326) were from Abcam, the rabbit polyclonal antibody RTN4 (10950-1-AP) was from Proteintech, the mouse anti-phosphoglycan (Galβ1,4Manα1-PO4) CA7AE monoclonal antibody ( ) was from Cedarlane, the rabbit anti-β-actin polyclonal antibody was from Cell Signalling, the rabbit anti-Tom20 polyclonal antibody (EPR15581-54) was from Abcam, and the rat anti-LAMP-1 monoclonal antibody 1D4B developed by J.T.

Techniques: Control, Infection, Comparison

TaqMan gene expression assay information (RhoA/ROCK pathway)

Journal: Journal of Neurophysiology

Article Title: Differential expression of genes in the RhoA/ROCK pathway in the hippocampus and cortex following intermittent hypoxia and high-intensity interval training

doi: 10.1152/jn.00422.2023

Figure Lengend Snippet: TaqMan gene expression assay information (RhoA/ROCK pathway)

Article Snippet: Inhibitory ligands , Nogo-A , Target , Rtn4 , Rn00582903_m1 , 90.

Techniques: Gene Expression, TaqMan Assay, Amplification, Membrane