Journal: Nature medicine

Article Title: ApoE attenuates unresolvable inflammation by complex formation with activated C1q

doi: 10.1038/s41591-018-0336-8

Figure Lengend Snippet: ( a ) ChPs were stained for complement C3 (red), anaphylatoxin C3a (cyan), and Ig (green). Bar 100 μm. ( b ) Complement C5. ChPs were stained for complement C5 (red). Bar 10 μm. ( c ) Liver-targeted C5-siRNA reduces serum C5. Control (n = 9 mice), C5 (n=9). ( d-f ) C5-siRNA attenuates leukocyte infiltration ( d ), CD68 + macrophage/DC infiltration ( e ), and CD3 + T cell infiltration ( f ) in ApoE -/- ChPs. Bars 10 μm. Control (n = 6 mice), C5 (6). ( g ) Low C4 and C3 protein levels in lipid deposits of HFD ApoE4 ChPs. Serial sections of ChPs as shown in were stained for C4 (green) and C3 (red). ( h ) Super-resolution (STED) microscopy shows colocalization of C1q (green) and ApoE (red) in HFD ApoE4 ChPs. Bar 10 μm. ( i ) ChP complement mRNA expression. WT (n=4 mice); ApoE -/- (n=5); ND ApoE3 (n=6); HFD ApoE3 (n=6); ND ApoE4 (n=6); HFD ApoE4 (n=6). Data in a,b,g,h are representative images from at least 3 independent mouse samples. Data represent means± SEM; Two-tailed Student´s t-test was applied to c,d,e,f. *** P <0.0001; one-way ANOVA with Tukey’s test was applied to i. Gene names in .

Article Snippet: Immunofluorescence staining was performed as previously described , using marker antibodies anti-mouse collagen IV (2150-1470; AbDSerotec), immunoglobulins (715-166-151; Dianova), immunoglobulin isotype that do not react with mouse Ig (017-160-006; Dianova), anti-human/mouse C3 (A213, ComplementTech), anti-human/mouse C3a (A218, ComplementTech), anti-human C5 (A220, ComplementTech), anti-mouse C5 (ab11898, Abcam), isotype for C5 (ab27478, Abcam), anti-mouse C1q (HM1096BT, Hycult Biotech), anti-human C1q (ab71089, Abcam), anti-mouse C4 (HM1046, Hycult Biotech), anti-human Factor H (A312, Quidel), anti-mouse Factor H (HM1119F, Hycult Biotech), anti-human ApoE (ab52607, Abcam), anti-human ApoE (178479; Calbiochem), anti-mouse ApoE (ab183597, Abcam), anti-mouse CD68 (FA11; Serotec), anti-human CD68 (EMB11, DAKO), anti-mouse CD31 (553370; BD PharMingen), anti-mouse iba-1 (019-19741; WAKO), anti-mouse CD45 (BZL 01145; Biozol), anti-human/mouse cytokeratin (Z0622; DAKO), anti-human collagen IV (CIV22, DAKO), anti-beta-amyloid (4G8, Biolegend), anti-phospho-Tau (AT8, Thermofisher), anti-iba1 (polyclonal, WAKO), anti-LAMP1 (1D4B, Abcam), TO-PRO™-3 Iodide (642/661) (T3605, Thermo Fisher Scientific) or DAPI for DNA.

Techniques: Staining, Microscopy, Expressing, Two Tailed Test

Journal: Nature medicine

Article Title: ApoE attenuates unresolvable inflammation by complex formation with activated C1q

doi: 10.1038/s41591-018-0336-8

Figure Lengend Snippet: ( a ) ChPs were stained for C1q (red) and C4 (green). Bar 100 µm. ( b ) C5 siRNA treatment blocks C5 protein deposition in ApoE-/- ChPs; ( c ) ChPs were stained for C3. Ig represents lipid; ( d ) Serum C3 and C5. Serum C3 and C5 protein levels were measured by ELISA. ApoE-/-(n = 6 mice), HFD ApoE4 (n=5). ( e ) High resolution confocal microscopy shows colocalization of ApoE4 (ApoE, red) and Ig (green, represents lipid) in HFD ApoE4-KI ChPs. ApoE-/- ChPs serve as negative controls for ApoE staining; ( f) Complement regulators are expressed in ChPs. WT (n = 5 mice); ApoE-/-(n=4); ND ApoE3 (n=6); HFD ApoE3 (n=6); ND ApoE4 (n=6); HFD ApoE4 (n=6). ( g ) ChP Factor H expressed between WT and ApoE-/- mice. WT (n=5); ApoE-/-(n=4); (h) ChP factor H protein in ChPs. White arrows indicate lipid positive areas. Data in a,b,c,e,h are representative images from at least 3 biologically independent mouse samples. Data in d,f,g represent means ± SEM; Two-tailed Student's t-test was applied to d,g; one-way ANOVA with Tukey posttest was applied to f; Gene names in .

Article Snippet: Immunofluorescence staining was performed as previously described , using marker antibodies anti-mouse collagen IV (2150-1470; AbDSerotec), immunoglobulins (715-166-151; Dianova), immunoglobulin isotype that do not react with mouse Ig (017-160-006; Dianova), anti-human/mouse C3 (A213, ComplementTech), anti-human/mouse C3a (A218, ComplementTech), anti-human C5 (A220, ComplementTech), anti-mouse C5 (ab11898, Abcam), isotype for C5 (ab27478, Abcam), anti-mouse C1q (HM1096BT, Hycult Biotech), anti-human C1q (ab71089, Abcam), anti-mouse C4 (HM1046, Hycult Biotech), anti-human Factor H (A312, Quidel), anti-mouse Factor H (HM1119F, Hycult Biotech), anti-human ApoE (ab52607, Abcam), anti-human ApoE (178479; Calbiochem), anti-mouse ApoE (ab183597, Abcam), anti-mouse CD68 (FA11; Serotec), anti-human CD68 (EMB11, DAKO), anti-mouse CD31 (553370; BD PharMingen), anti-mouse iba-1 (019-19741; WAKO), anti-mouse CD45 (BZL 01145; Biozol), anti-human/mouse cytokeratin (Z0622; DAKO), anti-human collagen IV (CIV22, DAKO), anti-beta-amyloid (4G8, Biolegend), anti-phospho-Tau (AT8, Thermofisher), anti-iba1 (polyclonal, WAKO), anti-LAMP1 (1D4B, Abcam), TO-PRO™-3 Iodide (642/661) (T3605, Thermo Fisher Scientific) or DAPI for DNA.

Techniques: Staining, Enzyme-linked Immunosorbent Assay, Confocal Microscopy, Two Tailed Test

Journal: Nature medicine

Article Title: ApoE attenuates unresolvable inflammation by complex formation with activated C1q

doi: 10.1038/s41591-018-0336-8

Figure Lengend Snippet: ( a ) Human ChP sections were stained with ORO/HE. Bar 100 μm. ChPs lipid was quantified as described in . Non-dementia cases (n=13) and demented cases (n=17). ( b ) Pearson correlation of ChP lipid and neurofibrillary tangle stage (Braak & Braak). n=30. ( c-e ) ChP lipid correlate with Aβ score (Thal phase), neuritic plaque score (CERAD), and ApoE4 genotype. n = 30 biologically independent samples, ( f ) ChP lipid correlates with dementia in ApoE3/ApoE3 carriers. ApoE3/ApoE3 Non-dementia cases (n=10) and demented cases (n=7). ( g ) Human ChP sections were stained for C1q (green) and C5 (red). Bar 100 μm. C5 percentage of lipid- ChP and lipid+ ChP from the same case was quantified according the Methods. Lipid- (n=7 biologically independent samples), lipid+ (n=7). ( h ) STED microscopy shows colocalization of C1q (green) and ApoE (red). Bar 5 μm. ( i ) Binding of C1q-ApoE in vivo by PLA. Anti-ApoE, anti-C1q, or no primary antibodies were used as controls. The number of C1q-ApoE complexes of lipid-negative ChP or lipid-positive areas were quantified as described in . Lipid- (n=4 independent samples), lipid+ (n=4). Bar 5 μm. ( j ) Human brain sections were stained for Aβ/ApoE, pTau/ApoE, C1q/ApoE, or C1q alone. Protein-protein binding in vivo was detected by PLA. Blue for nuclei. Bar 5 μm. ( k ) 16 weeks AD (APPPS1-21) brain cortex sections were examined by the PLA assay for the presence of C1q/ApoE complexes, methoxy X04 to outline plaques. X04-(5), X04+ (5). Bars represent 10 μm. ( l ) Liver-targeted C5 siRNA reduces serum C5 in APPPS1-21 mice. Ctr (n=4 mice), C5 (n=5). ( m ) Brain sections were stained with iba1 for microglial cells (red), To-Pro-3 for nuclei, and X04 for Aβ plaque. White dashed circle represents the area within a 30 μm radius. The number of iba1 + /To-Pro-3 + cells per areawere quantified (> 30 μm radius represents non-Aβ plaque area). Plaques were further grouped into small plaques (X04% < 10% of 30 μm radius area), moderate plaques (X04% between 10 - 30% 30 μm radius area), and large plaques (X04% > 30% of 30 μm radius area). Percentage of iba1 positivity within a 30 μm radius of Aβ plaques and non-Aβ plaque areas were compared. 420 individual Aβ plaques and 40 fields of non-Aβ plaques from 4 control mice, 536 individual Aβ plaques and 51 fields of non-Aβ plaques from 5 C5 treated mice. Data in h,j are representative images from at least 3 independent samples. Data represent means ± SEM. Two-tailed Student´s t-test was applied to a,c,d,f; paired two-tailed Student´s t-test was applied to g,I,k; One-way ANOVA was applied to e; Two-way ANOVA was applied to l,m.

Article Snippet: Immunofluorescence staining was performed as previously described , using marker antibodies anti-mouse collagen IV (2150-1470; AbDSerotec), immunoglobulins (715-166-151; Dianova), immunoglobulin isotype that do not react with mouse Ig (017-160-006; Dianova), anti-human/mouse C3 (A213, ComplementTech), anti-human/mouse C3a (A218, ComplementTech), anti-human C5 (A220, ComplementTech), anti-mouse C5 (ab11898, Abcam), isotype for C5 (ab27478, Abcam), anti-mouse C1q (HM1096BT, Hycult Biotech), anti-human C1q (ab71089, Abcam), anti-mouse C4 (HM1046, Hycult Biotech), anti-human Factor H (A312, Quidel), anti-mouse Factor H (HM1119F, Hycult Biotech), anti-human ApoE (ab52607, Abcam), anti-human ApoE (178479; Calbiochem), anti-mouse ApoE (ab183597, Abcam), anti-mouse CD68 (FA11; Serotec), anti-human CD68 (EMB11, DAKO), anti-mouse CD31 (553370; BD PharMingen), anti-mouse iba-1 (019-19741; WAKO), anti-mouse CD45 (BZL 01145; Biozol), anti-human/mouse cytokeratin (Z0622; DAKO), anti-human collagen IV (CIV22, DAKO), anti-beta-amyloid (4G8, Biolegend), anti-phospho-Tau (AT8, Thermofisher), anti-iba1 (polyclonal, WAKO), anti-LAMP1 (1D4B, Abcam), TO-PRO™-3 Iodide (642/661) (T3605, Thermo Fisher Scientific) or DAPI for DNA.

Techniques: Staining, Microscopy, Binding Assay, In Vivo, Protein Binding, Two Tailed Test

Journal: Nature medicine

Article Title: ApoE attenuates unresolvable inflammation by complex formation with activated C1q

doi: 10.1038/s41591-018-0336-8

Figure Lengend Snippet: ( a )16 weeks APPPS1-21 mouse brain sections were stained with Aβ/ApoE complexes (red) by PLA, methoxy X04 for Aβ plaque (blue). High resolution confocal images show the spatial location of Aβ-ApoE complexes and Aβ plaque in 3D view (lower panel). Bars represent 10 µm. ( b ) Brain sections were stained with methoxy-X04, ApoE, and LAMP1; the size of areas covered by methoxy-X04, ApoE, and LAMP1 was determined. ApoE/X04 and LAMP1/X04 (X04 > 150 µm2) were quantified. n = 123 plaques from 4 control mice, 147 plaques from 5 treated mice. Bars 100 µm. ( c ) Aβ plaque was stained with methoxy X04 (X04). Number of plaques per section and number of plaque per area were quantified. control (n=4 mice), C5 (n=5). Bar 1000 µm; ( d ) Total plaque volume was determined in 3D, plaques were further grouped according to the plaque volume. n = 71 random fields from 4 control mice, 88 fields from 5 C5 treated mice. Bar 100 µm; ( e ) 8-week old C57BL6 brain cortex sections were examined for the presence of C1q-ApoE complexes with methoxy X04. ApoE, or C1q only antisera were used as negative controls. Bar represents 10 µm. Data in a,e are representative images from at least 3 biologically independent mouse samples. Data in b,c,d represent means ± SEM; two-tailed Student's t-test was applied to b,c,d; Two-way ANOVA was applied to c,d.

Article Snippet: Immunofluorescence staining was performed as previously described , using marker antibodies anti-mouse collagen IV (2150-1470; AbDSerotec), immunoglobulins (715-166-151; Dianova), immunoglobulin isotype that do not react with mouse Ig (017-160-006; Dianova), anti-human/mouse C3 (A213, ComplementTech), anti-human/mouse C3a (A218, ComplementTech), anti-human C5 (A220, ComplementTech), anti-mouse C5 (ab11898, Abcam), isotype for C5 (ab27478, Abcam), anti-mouse C1q (HM1096BT, Hycult Biotech), anti-human C1q (ab71089, Abcam), anti-mouse C4 (HM1046, Hycult Biotech), anti-human Factor H (A312, Quidel), anti-mouse Factor H (HM1119F, Hycult Biotech), anti-human ApoE (ab52607, Abcam), anti-human ApoE (178479; Calbiochem), anti-mouse ApoE (ab183597, Abcam), anti-mouse CD68 (FA11; Serotec), anti-human CD68 (EMB11, DAKO), anti-mouse CD31 (553370; BD PharMingen), anti-mouse iba-1 (019-19741; WAKO), anti-mouse CD45 (BZL 01145; Biozol), anti-human/mouse cytokeratin (Z0622; DAKO), anti-human collagen IV (CIV22, DAKO), anti-beta-amyloid (4G8, Biolegend), anti-phospho-Tau (AT8, Thermofisher), anti-iba1 (polyclonal, WAKO), anti-LAMP1 (1D4B, Abcam), TO-PRO™-3 Iodide (642/661) (T3605, Thermo Fisher Scientific) or DAPI for DNA.

Techniques: Staining, Two Tailed Test

Journal: Nature medicine

Article Title: ApoE attenuates unresolvable inflammation by complex formation with activated C1q

doi: 10.1038/s41591-018-0336-8

Figure Lengend Snippet: ( a ) Aorta complement gene mRNA expression. 6 weeks WT (n=3 mice); 32 weeks WT (n=3); 6 weeks ApoE -/- (n=3); 32 weeks ApoE -/- (n=3); ( b ) Liver-targeted C5 siRNA reduces serum C5 in young ApoE -/- mice. Ctr (n=11 mice), C5 (12). ( c ) En face staining for whole aorta. Bar 0.5 cm. Atherosclerotic plaques were quantified as described in . Control (n=11 mice), C5 siRNA (n=12). ( d , e ) Aortic root sections were stained for ORO/HE and CD68 + macrophages/DCs. Bars 100 μm. Plaque size ( d ) and CD68 + macrophages/DCs size ( e ) were quantified as described in . Control (n=4 mice), C5-siRNA (n=4). ( f ) Human carotid artery parallel sections were stained for CD68, C1q, ApoE, and C5 by DAB and hematoxylin. Representative images from g. ( g ) CD68, C1q, ApoE, and C5 signal was quantify as described in . Control (n=5 independent samples), early plaque (n=6), advanced plaque (n=9). ( h ) C1q-ApoE complexes in human atherosclerosis plaque was determined by PLA. Intima (n=3 independent samples), media (3). Bar 5 μm. ( i ) High resolution microscopy shows colocalization of lipid (green) and malondialdehyde epitopes (MDA2, red) in human atherosclerotic plaque. Bar 10 μm. Representative images from at least 3 independent samples. ( j ) Schematic representation of the C1q-ApoE complex. Locally produced and/or serum-recruited C1q is activated in situ by a variety of surface activators including oxidized lipid, oxidized LDL, amyloid fibrils, and immunoglobulins. C1q activators have been implicated in diseases as varied as atherosclerosis and AD. Following activation, C1q acquires an active conformation that allows initiation of the CCC with resultant generation of C3a and C3b and C5 cleavage to generate C5a and C5b. ApoE inhibits the CCC activity by binding of ApoE at high affinity to the active C1q and forms the C1q-ApoE complex (upper part of the panel). By contrast, inflammation is amplified in the absence of ApoE by overactivation of the CCC (lower panel). C1q: inactive (yellow); activated (light green); overactivated (red). Data represent means ± SEM. Two-tailed Student´s t-test was applied to b,c,h; One-way ANOVA was applied to a,g; Two-way ANOVA was applied to d,e.

Article Snippet: Immunofluorescence staining was performed as previously described , using marker antibodies anti-mouse collagen IV (2150-1470; AbDSerotec), immunoglobulins (715-166-151; Dianova), immunoglobulin isotype that do not react with mouse Ig (017-160-006; Dianova), anti-human/mouse C3 (A213, ComplementTech), anti-human/mouse C3a (A218, ComplementTech), anti-human C5 (A220, ComplementTech), anti-mouse C5 (ab11898, Abcam), isotype for C5 (ab27478, Abcam), anti-mouse C1q (HM1096BT, Hycult Biotech), anti-human C1q (ab71089, Abcam), anti-mouse C4 (HM1046, Hycult Biotech), anti-human Factor H (A312, Quidel), anti-mouse Factor H (HM1119F, Hycult Biotech), anti-human ApoE (ab52607, Abcam), anti-human ApoE (178479; Calbiochem), anti-mouse ApoE (ab183597, Abcam), anti-mouse CD68 (FA11; Serotec), anti-human CD68 (EMB11, DAKO), anti-mouse CD31 (553370; BD PharMingen), anti-mouse iba-1 (019-19741; WAKO), anti-mouse CD45 (BZL 01145; Biozol), anti-human/mouse cytokeratin (Z0622; DAKO), anti-human collagen IV (CIV22, DAKO), anti-beta-amyloid (4G8, Biolegend), anti-phospho-Tau (AT8, Thermofisher), anti-iba1 (polyclonal, WAKO), anti-LAMP1 (1D4B, Abcam), TO-PRO™-3 Iodide (642/661) (T3605, Thermo Fisher Scientific) or DAPI for DNA.

Techniques: Expressing, Staining, Microscopy, Produced, In Situ, Activation Assay, Activity Assay, Binding Assay, Amplification, Two Tailed Test

Journal: Nature medicine

Article Title: ApoE attenuates unresolvable inflammation by complex formation with activated C1q

doi: 10.1038/s41591-018-0336-8

Figure Lengend Snippet: ( a ) Expression microarray analyses of aortas. Heatmaps show GO terms leukocyte migration, complement activation, phagocytosis, and cellular response to lipid. 6 weeks WT (n=3 mice); 32 weeks WT (n=3); 6 weeks ApoE-/- (n=3); 32 weeks ApoE-/- (n=3); ( b ) aorta alternative complement pathway genes (factor B, factor H, factor D) mRNA expression in 6 weeks and 32 weeks old WT and ApoE-/- mouse aortas. 6 weeks WT (n=3 mice); 32 weeks WT (n=3); 6 weeks ApoE-/- (n=3); 32 weeks ApoE-/- (n=3); ( c - d ) plasma cholesterol and body weight; ( e - f ) blood leukocytes and percentage. For c-f, control (11 mice); C5 siRNA (12 mice). ( g ) blood CD4+ T cells, CD8+ T cells, and B220+ B cells by flow cytometry. Control (6 mice); C5 siRNA (6 mice). ( h ) super-resolution microscopy shows colocalization of C1q (green) and ApoE (red) in human atherosclerotic plaque. Representative images from at least 3 biologically independent mouse samples. Bar 5 µm. Data in b,c,d,e,f,g represent means ± SEM; Two-tailed Student's t-test was applied to c.d.e.f.g; one-way ANOVA with Tukey posttest was applied to b; abbreviations: WBC, white blood cells; RBC, red blood cells; PLT, platelets; LYM, lymphocytes; MO, monocytes; GRA, granulocytes. Gene names and statistics in .

Article Snippet: Immunofluorescence staining was performed as previously described , using marker antibodies anti-mouse collagen IV (2150-1470; AbDSerotec), immunoglobulins (715-166-151; Dianova), immunoglobulin isotype that do not react with mouse Ig (017-160-006; Dianova), anti-human/mouse C3 (A213, ComplementTech), anti-human/mouse C3a (A218, ComplementTech), anti-human C5 (A220, ComplementTech), anti-mouse C5 (ab11898, Abcam), isotype for C5 (ab27478, Abcam), anti-mouse C1q (HM1096BT, Hycult Biotech), anti-human C1q (ab71089, Abcam), anti-mouse C4 (HM1046, Hycult Biotech), anti-human Factor H (A312, Quidel), anti-mouse Factor H (HM1119F, Hycult Biotech), anti-human ApoE (ab52607, Abcam), anti-human ApoE (178479; Calbiochem), anti-mouse ApoE (ab183597, Abcam), anti-mouse CD68 (FA11; Serotec), anti-human CD68 (EMB11, DAKO), anti-mouse CD31 (553370; BD PharMingen), anti-mouse iba-1 (019-19741; WAKO), anti-mouse CD45 (BZL 01145; Biozol), anti-human/mouse cytokeratin (Z0622; DAKO), anti-human collagen IV (CIV22, DAKO), anti-beta-amyloid (4G8, Biolegend), anti-phospho-Tau (AT8, Thermofisher), anti-iba1 (polyclonal, WAKO), anti-LAMP1 (1D4B, Abcam), TO-PRO™-3 Iodide (642/661) (T3605, Thermo Fisher Scientific) or DAPI for DNA.

Techniques: Expressing, Microarray, Migration, Activation Assay, Flow Cytometry, Microscopy, Two Tailed Test

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Cellular retinol binding protein 1 could be a tumor suppressor gene in cervical cancer

doi:

Figure Lengend Snippet: Molecular events for CRBP1 gene in cervical epithelium samples. A: In order to know the gain of copy number of the CRBP1 gene, DNA of healthy cervix and CC samples, were subjected to real time PCR with specific Taqman probes. White bar (healthy cervix samples) represents the mean of the normal cervices (n = 26) without extra copies of CRBP1 gene. Black bars show CC samples with gain of copy number (2-20X); while gray dotted line bars are showing CC samples that do not change in the copies number. Values above the cut-off line (as 1), being assigned as increased gene copy number compared with normal cervical epithelium. CRBP1 Hs01437985_cn probe, and Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) Hs00894322_cn probe were used as reference; the relative genomic copy number was calculated using the comparative Ct methods [26]. In X-axis represents cervical samples, Y-axis relative copies fold change of CRBP1 gene. B: CRBP1 expression was observed as positive immunostaining result on tissue microarray as mentioned in Methods section The DNAs used for gain of copy number (panel A) were also used for the methylation assay. Methylation result represents the methylation of the CRBP1 promoter. In this case, each healthy or CC sample, correspond to each column for CRBP1 expression and methylation status. Interestingly, in most of the cases, there was an association between the lack of expression of the CRBP1 gene and its methylation status.

Article Snippet: Incubation with the monoclonal mouse anti-CRBP1 antibody (ab24090 Abcam) was performed overnight at 4°C, at 1:100 dilution in 1% bovine serum albumin in phosphate buffered saline (PBS).

Techniques: Real-time Polymerase Chain Reaction, Expressing, Immunostaining, Microarray, Methylation

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Cellular retinol binding protein 1 could be a tumor suppressor gene in cervical cancer

doi:

Figure Lengend Snippet: CRBP1 immunodetection in the uterine cervix samples. A: (1) Cytoplasmic CRBP1 expression is present in cells of the basal layer of normal cervical epithelium (healthy tissue); (2) the immunodetection in the transformed cells of a cervical cancer (CC03) tissue harboring gain of CRBP1 gene. (3) CC samples without gain CRBP1 gene showing negative immunostaining (CC16 sample). A kidney tissue section (4) was used as positive control, while a heart tissue section for negative control (5). B: cervical progression spectrum. The tissue section shows a brownish reaction (positive reaction) in the basal cell layer of the “normal” region, in the high-grade lesion, and also in the invasive region. All tissue sections were hematoxylin counterstained, 200X original amplification.

Article Snippet: Incubation with the monoclonal mouse anti-CRBP1 antibody (ab24090 Abcam) was performed overnight at 4°C, at 1:100 dilution in 1% bovine serum albumin in phosphate buffered saline (PBS).

Techniques: Immunodetection, Expressing, Transformation Assay, Immunostaining, Positive Control, Negative Control, Amplification

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Cellular retinol binding protein 1 could be a tumor suppressor gene in cervical cancer

doi:

Figure Lengend Snippet: Association between CRBP1 gene gain copy number and its expression in cervical cancer samples

Article Snippet: Incubation with the monoclonal mouse anti-CRBP1 antibody (ab24090 Abcam) was performed overnight at 4°C, at 1:100 dilution in 1% bovine serum albumin in phosphate buffered saline (PBS).

Techniques: Expressing, Immunodetection

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Cellular retinol binding protein 1 could be a tumor suppressor gene in cervical cancer

doi:

Figure Lengend Snippet: Correlation between CRBP1 expression and clinic pathological variables in cervical cancer

Article Snippet: Incubation with the monoclonal mouse anti-CRBP1 antibody (ab24090 Abcam) was performed overnight at 4°C, at 1:100 dilution in 1% bovine serum albumin in phosphate buffered saline (PBS).

Techniques: Expressing, Activity Assay

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Cellular retinol binding protein 1 could be a tumor suppressor gene in cervical cancer

doi:

Figure Lengend Snippet: Immunolocalization of CRBP1 by immunofluorescence in cervical cells. Nuclei were Dapi stained in blue color (A-C). The immunodetection of CRBP1 was observed in green color (D-F). Cytoplasmic immunodetection of CRBP1 in the merge imaging (G-I). 100X original amplification.

Article Snippet: Incubation with the monoclonal mouse anti-CRBP1 antibody (ab24090 Abcam) was performed overnight at 4°C, at 1:100 dilution in 1% bovine serum albumin in phosphate buffered saline (PBS).

Techniques: Immunofluorescence, Staining, Immunodetection, Imaging, Amplification

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Cellular retinol binding protein 1 could be a tumor suppressor gene in cervical cancer

doi:

Figure Lengend Snippet: Methylation promoter of CRBP1 gene in cervical cancer samples. Example of CRBP1 gene promoter methylation analysis. Lanes: Healthy cervix sample, CC03 and CC06 samples with un-methylated status; lanes CC 10 and CC 16 with methylated status; HeLa cells as un-methylated control (109 bp), or MCF-7 cells as methylated control (99 bp). MW: molecular weight marker of 100 bp.

Article Snippet: Incubation with the monoclonal mouse anti-CRBP1 antibody (ab24090 Abcam) was performed overnight at 4°C, at 1:100 dilution in 1% bovine serum albumin in phosphate buffered saline (PBS).

Techniques: Methylation, Molecular Weight, Marker

Journal: Cell Death and Differentiation

Article Title: Inhibition of cGAS-STING by JQ1 alleviates oxidative stress-induced retina inflammation and degeneration

doi: 10.1038/s41418-022-00967-4

Figure Lengend Snippet: Key reagents and resources used in this study.

Article Snippet: TBK1/NAK (D1B4) Rabbit mAb , Cell Signaling Technology , cat#3504.

Techniques: Marker, Recombinant, Transfection, Drug discovery, Gene Expression, Microarray, Software

Journal: Cell stem cell

Article Title: A M etformin -R esponsive M etabolic P athway controls distinct steps in gastric progenitor fate decisions and maturation

doi: 10.1016/j.stem.2020.03.006

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: Vectastain Elite ABC HRP Kit , Vector Laboratories , Cat#PK6100.

Techniques: Recombinant, SYBR Green Assay, Protein Extraction, Plasmid Preparation, Microarray, Expressing, Software, Imaging