whole mouse genome microarray kit (4 × 44k Search Results


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Abcam monoclonal mouse anti crbp1 antibody
Molecular events for <t>CRBP1</t> 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.
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TaKaRa e1910 thruplex dna seq kit takara
Molecular events for <t>CRBP1</t> 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.
E1910 Thruplex Dna Seq Kit Takara, supplied by TaKaRa, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Agilent technologies mouse genome cgh microarray kit 244a
RNA from sensitive tumors treated with either vehicle or NVP-LDE225 (20mg/kg/day) for 4, 16 and 48 hours, and resistant tumors treated with 20 or 160 mg/kg/day (mpk) for 26 days (d) was profiled on Affymetrix mouse gene expression arrays. A, Pattern of genes initially inhibited by NVP-LDE225 but reemerging in resistant tumors. Numbers express relative rank in expression. B, Top ranking genes by Spearman correlation of expression matching with the pattern in 2A. C, Heat map of the top ranked genes associated with the pattern in 2A. Each gene’s expression values are z-transformed for comparability, with red indicating relatively high expression and green indicating relatively low expression. D, <t>CGH</t> analysis using the Agilent Mouse Genome CGH <t>Microarray</t> Kit <t>244A</t> of three resistant (LDE 1,2,3) and three sensitive (Veh 1,2,3) tumors identified a focal amplification in the region containing Gli2 on Chromosome 1 in 2 out of 3 resistant tumors. Copy number changes are expressed as log2. E, Additional DNA from normal liver (NL), vehicle (controls) and resistant tumors was analyzed by quantitative PCR for the Gli2 locus. F, Correlation between levels of Gli2 mRNA expression and Gli2 copy number is shown for vehicle-treated control tumors (open square) and resistant tumors that emerged after treatment with NVP-LDE225 at 10 bid (green square), 20 qd (red diamond), 40 bid (brown triangle), 80 bid (blue circle) and 160 bid (black inverse triangle) mg/kg/day. Axis in log10 scale. G, Inhibition of Gli2 mRNA levels by siRNA knock-down of Gli2 was associated with decreased proliferation and Gli1 mRNA expression in resistant Gli2 amplified (copy number:20) and Gli2-overexpressing (17-fold) medulloblastoma tumors. Two independent Gli2 siRNAs (Gli2-1 and Gli2-1) were used.
Mouse Genome Cgh Microarray Kit 244a, supplied by Agilent technologies, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Invent Biotechnologies cell fractionation kit invent biotechnologies cat
RNA from sensitive tumors treated with either vehicle or NVP-LDE225 (20mg/kg/day) for 4, 16 and 48 hours, and resistant tumors treated with 20 or 160 mg/kg/day (mpk) for 26 days (d) was profiled on Affymetrix mouse gene expression arrays. A, Pattern of genes initially inhibited by NVP-LDE225 but reemerging in resistant tumors. Numbers express relative rank in expression. B, Top ranking genes by Spearman correlation of expression matching with the pattern in 2A. C, Heat map of the top ranked genes associated with the pattern in 2A. Each gene’s expression values are z-transformed for comparability, with red indicating relatively high expression and green indicating relatively low expression. D, <t>CGH</t> analysis using the Agilent Mouse Genome CGH <t>Microarray</t> Kit <t>244A</t> of three resistant (LDE 1,2,3) and three sensitive (Veh 1,2,3) tumors identified a focal amplification in the region containing Gli2 on Chromosome 1 in 2 out of 3 resistant tumors. Copy number changes are expressed as log2. E, Additional DNA from normal liver (NL), vehicle (controls) and resistant tumors was analyzed by quantitative PCR for the Gli2 locus. F, Correlation between levels of Gli2 mRNA expression and Gli2 copy number is shown for vehicle-treated control tumors (open square) and resistant tumors that emerged after treatment with NVP-LDE225 at 10 bid (green square), 20 qd (red diamond), 40 bid (brown triangle), 80 bid (blue circle) and 160 bid (black inverse triangle) mg/kg/day. Axis in log10 scale. G, Inhibition of Gli2 mRNA levels by siRNA knock-down of Gli2 was associated with decreased proliferation and Gli1 mRNA expression in resistant Gli2 amplified (copy number:20) and Gli2-overexpressing (17-fold) medulloblastoma tumors. Two independent Gli2 siRNAs (Gli2-1 and Gli2-1) were used.
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Vector Laboratories immpress hrp anti mouse igg
RNA from sensitive tumors treated with either vehicle or NVP-LDE225 (20mg/kg/day) for 4, 16 and 48 hours, and resistant tumors treated with 20 or 160 mg/kg/day (mpk) for 26 days (d) was profiled on Affymetrix mouse gene expression arrays. A, Pattern of genes initially inhibited by NVP-LDE225 but reemerging in resistant tumors. Numbers express relative rank in expression. B, Top ranking genes by Spearman correlation of expression matching with the pattern in 2A. C, Heat map of the top ranked genes associated with the pattern in 2A. Each gene’s expression values are z-transformed for comparability, with red indicating relatively high expression and green indicating relatively low expression. D, <t>CGH</t> analysis using the Agilent Mouse Genome CGH <t>Microarray</t> Kit <t>244A</t> of three resistant (LDE 1,2,3) and three sensitive (Veh 1,2,3) tumors identified a focal amplification in the region containing Gli2 on Chromosome 1 in 2 out of 3 resistant tumors. Copy number changes are expressed as log2. E, Additional DNA from normal liver (NL), vehicle (controls) and resistant tumors was analyzed by quantitative PCR for the Gli2 locus. F, Correlation between levels of Gli2 mRNA expression and Gli2 copy number is shown for vehicle-treated control tumors (open square) and resistant tumors that emerged after treatment with NVP-LDE225 at 10 bid (green square), 20 qd (red diamond), 40 bid (brown triangle), 80 bid (blue circle) and 160 bid (black inverse triangle) mg/kg/day. Axis in log10 scale. G, Inhibition of Gli2 mRNA levels by siRNA knock-down of Gli2 was associated with decreased proliferation and Gli1 mRNA expression in resistant Gli2 amplified (copy number:20) and Gli2-overexpressing (17-fold) medulloblastoma tumors. Two independent Gli2 siRNAs (Gli2-1 and Gli2-1) were used.
Immpress Hrp Anti Mouse Igg, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Qiagen rneasy mini kit
RNA from sensitive tumors treated with either vehicle or NVP-LDE225 (20mg/kg/day) for 4, 16 and 48 hours, and resistant tumors treated with 20 or 160 mg/kg/day (mpk) for 26 days (d) was profiled on Affymetrix mouse gene expression arrays. A, Pattern of genes initially inhibited by NVP-LDE225 but reemerging in resistant tumors. Numbers express relative rank in expression. B, Top ranking genes by Spearman correlation of expression matching with the pattern in 2A. C, Heat map of the top ranked genes associated with the pattern in 2A. Each gene’s expression values are z-transformed for comparability, with red indicating relatively high expression and green indicating relatively low expression. D, <t>CGH</t> analysis using the Agilent Mouse Genome CGH <t>Microarray</t> Kit <t>244A</t> of three resistant (LDE 1,2,3) and three sensitive (Veh 1,2,3) tumors identified a focal amplification in the region containing Gli2 on Chromosome 1 in 2 out of 3 resistant tumors. Copy number changes are expressed as log2. E, Additional DNA from normal liver (NL), vehicle (controls) and resistant tumors was analyzed by quantitative PCR for the Gli2 locus. F, Correlation between levels of Gli2 mRNA expression and Gli2 copy number is shown for vehicle-treated control tumors (open square) and resistant tumors that emerged after treatment with NVP-LDE225 at 10 bid (green square), 20 qd (red diamond), 40 bid (brown triangle), 80 bid (blue circle) and 160 bid (black inverse triangle) mg/kg/day. Axis in log10 scale. G, Inhibition of Gli2 mRNA levels by siRNA knock-down of Gli2 was associated with decreased proliferation and Gli1 mRNA expression in resistant Gli2 amplified (copy number:20) and Gli2-overexpressing (17-fold) medulloblastoma tumors. Two independent Gli2 siRNAs (Gli2-1 and Gli2-1) were used.
Rneasy Mini Kit, supplied by Qiagen, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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RNA from sensitive tumors treated with either vehicle or NVP-LDE225 (20mg/kg/day) for 4, 16 and 48 hours, and resistant tumors treated with 20 or 160 mg/kg/day (mpk) for 26 days (d) was profiled on Affymetrix mouse gene expression arrays. A, Pattern of genes initially inhibited by NVP-LDE225 but reemerging in resistant tumors. Numbers express relative rank in expression. B, Top ranking genes by Spearman correlation of expression matching with the pattern in 2A. C, Heat map of the top ranked genes associated with the pattern in 2A. Each gene’s expression values are z-transformed for comparability, with red indicating relatively high expression and green indicating relatively low expression. D, <t>CGH</t> analysis using the Agilent Mouse Genome CGH <t>Microarray</t> Kit <t>244A</t> of three resistant (LDE 1,2,3) and three sensitive (Veh 1,2,3) tumors identified a focal amplification in the region containing Gli2 on Chromosome 1 in 2 out of 3 resistant tumors. Copy number changes are expressed as log2. E, Additional DNA from normal liver (NL), vehicle (controls) and resistant tumors was analyzed by quantitative PCR for the Gli2 locus. F, Correlation between levels of Gli2 mRNA expression and Gli2 copy number is shown for vehicle-treated control tumors (open square) and resistant tumors that emerged after treatment with NVP-LDE225 at 10 bid (green square), 20 qd (red diamond), 40 bid (brown triangle), 80 bid (blue circle) and 160 bid (black inverse triangle) mg/kg/day. Axis in log10 scale. G, Inhibition of Gli2 mRNA levels by siRNA knock-down of Gli2 was associated with decreased proliferation and Gli1 mRNA expression in resistant Gli2 amplified (copy number:20) and Gli2-overexpressing (17-fold) medulloblastoma tumors. Two independent Gli2 siRNAs (Gli2-1 and Gli2-1) were used.
Rneasy Plus Micro Kit Qiagen, supplied by Qiagen, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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RNA from sensitive tumors treated with either vehicle or NVP-LDE225 (20mg/kg/day) for 4, 16 and 48 hours, and resistant tumors treated with 20 or 160 mg/kg/day (mpk) for 26 days (d) was profiled on Affymetrix mouse gene expression arrays. A, Pattern of genes initially inhibited by NVP-LDE225 but reemerging in resistant tumors. Numbers express relative rank in expression. B, Top ranking genes by Spearman correlation of expression matching with the pattern in 2A. C, Heat map of the top ranked genes associated with the pattern in 2A. Each gene’s expression values are z-transformed for comparability, with red indicating relatively high expression and green indicating relatively low expression. D, <t>CGH</t> analysis using the Agilent Mouse Genome CGH <t>Microarray</t> Kit <t>244A</t> of three resistant (LDE 1,2,3) and three sensitive (Veh 1,2,3) tumors identified a focal amplification in the region containing Gli2 on Chromosome 1 in 2 out of 3 resistant tumors. Copy number changes are expressed as log2. E, Additional DNA from normal liver (NL), vehicle (controls) and resistant tumors was analyzed by quantitative PCR for the Gli2 locus. F, Correlation between levels of Gli2 mRNA expression and Gli2 copy number is shown for vehicle-treated control tumors (open square) and resistant tumors that emerged after treatment with NVP-LDE225 at 10 bid (green square), 20 qd (red diamond), 40 bid (brown triangle), 80 bid (blue circle) and 160 bid (black inverse triangle) mg/kg/day. Axis in log10 scale. G, Inhibition of Gli2 mRNA levels by siRNA knock-down of Gli2 was associated with decreased proliferation and Gli1 mRNA expression in resistant Gli2 amplified (copy number:20) and Gli2-overexpressing (17-fold) medulloblastoma tumors. Two independent Gli2 siRNAs (Gli2-1 and Gli2-1) were used.
Rneasy Microkit, supplied by Qiagen, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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RNA from sensitive tumors treated with either vehicle or NVP-LDE225 (20mg/kg/day) for 4, 16 and 48 hours, and resistant tumors treated with 20 or 160 mg/kg/day (mpk) for 26 days (d) was profiled on Affymetrix mouse gene expression arrays. A, Pattern of genes initially inhibited by NVP-LDE225 but reemerging in resistant tumors. Numbers express relative rank in expression. B, Top ranking genes by Spearman correlation of expression matching with the pattern in 2A. C, Heat map of the top ranked genes associated with the pattern in 2A. Each gene’s expression values are z-transformed for comparability, with red indicating relatively high expression and green indicating relatively low expression. D, <t>CGH</t> analysis using the Agilent Mouse Genome CGH <t>Microarray</t> Kit <t>244A</t> of three resistant (LDE 1,2,3) and three sensitive (Veh 1,2,3) tumors identified a focal amplification in the region containing Gli2 on Chromosome 1 in 2 out of 3 resistant tumors. Copy number changes are expressed as log2. E, Additional DNA from normal liver (NL), vehicle (controls) and resistant tumors was analyzed by quantitative PCR for the Gli2 locus. F, Correlation between levels of Gli2 mRNA expression and Gli2 copy number is shown for vehicle-treated control tumors (open square) and resistant tumors that emerged after treatment with NVP-LDE225 at 10 bid (green square), 20 qd (red diamond), 40 bid (brown triangle), 80 bid (blue circle) and 160 bid (black inverse triangle) mg/kg/day. Axis in log10 scale. G, Inhibition of Gli2 mRNA levels by siRNA knock-down of Gli2 was associated with decreased proliferation and Gli1 mRNA expression in resistant Gli2 amplified (copy number:20) and Gli2-overexpressing (17-fold) medulloblastoma tumors. Two independent Gli2 siRNAs (Gli2-1 and Gli2-1) were used.
Rneasy Kit, supplied by Qiagen, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Journal: eLife

Article Title: Evaluating the transcriptional regulators of arterial gene expression via a catalogue of characterized arterial enhancers

doi: 10.7554/eLife.102440

Figure Lengend Snippet:

Article Snippet: Commercial assay or kit , ChIP DNA Clean & Concentrator kit , Zymo Research , D5205 , .

Techniques: Recombinant, Control, Multiplex Assay, TA Cloning, Software

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.

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

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.

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

Association between  CRBP1  gene gain copy number and its expression in cervical cancer samples

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

Correlation between  CRBP1  expression and clinic pathological variables in cervical cancer

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

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.

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

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.

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

RNA from sensitive tumors treated with either vehicle or NVP-LDE225 (20mg/kg/day) for 4, 16 and 48 hours, and resistant tumors treated with 20 or 160 mg/kg/day (mpk) for 26 days (d) was profiled on Affymetrix mouse gene expression arrays. A, Pattern of genes initially inhibited by NVP-LDE225 but reemerging in resistant tumors. Numbers express relative rank in expression. B, Top ranking genes by Spearman correlation of expression matching with the pattern in 2A. C, Heat map of the top ranked genes associated with the pattern in 2A. Each gene’s expression values are z-transformed for comparability, with red indicating relatively high expression and green indicating relatively low expression. D, CGH analysis using the Agilent Mouse Genome CGH Microarray Kit 244A of three resistant (LDE 1,2,3) and three sensitive (Veh 1,2,3) tumors identified a focal amplification in the region containing Gli2 on Chromosome 1 in 2 out of 3 resistant tumors. Copy number changes are expressed as log2. E, Additional DNA from normal liver (NL), vehicle (controls) and resistant tumors was analyzed by quantitative PCR for the Gli2 locus. F, Correlation between levels of Gli2 mRNA expression and Gli2 copy number is shown for vehicle-treated control tumors (open square) and resistant tumors that emerged after treatment with NVP-LDE225 at 10 bid (green square), 20 qd (red diamond), 40 bid (brown triangle), 80 bid (blue circle) and 160 bid (black inverse triangle) mg/kg/day. Axis in log10 scale. G, Inhibition of Gli2 mRNA levels by siRNA knock-down of Gli2 was associated with decreased proliferation and Gli1 mRNA expression in resistant Gli2 amplified (copy number:20) and Gli2-overexpressing (17-fold) medulloblastoma tumors. Two independent Gli2 siRNAs (Gli2-1 and Gli2-1) were used.

Journal: Science translational medicine

Article Title: Interfering with Resistance to Smoothened Antagonists by Inhibition of the PI3K Pathway in Medulloblastoma

doi: 10.1126/scitranslmed.3001599

Figure Lengend Snippet: RNA from sensitive tumors treated with either vehicle or NVP-LDE225 (20mg/kg/day) for 4, 16 and 48 hours, and resistant tumors treated with 20 or 160 mg/kg/day (mpk) for 26 days (d) was profiled on Affymetrix mouse gene expression arrays. A, Pattern of genes initially inhibited by NVP-LDE225 but reemerging in resistant tumors. Numbers express relative rank in expression. B, Top ranking genes by Spearman correlation of expression matching with the pattern in 2A. C, Heat map of the top ranked genes associated with the pattern in 2A. Each gene’s expression values are z-transformed for comparability, with red indicating relatively high expression and green indicating relatively low expression. D, CGH analysis using the Agilent Mouse Genome CGH Microarray Kit 244A of three resistant (LDE 1,2,3) and three sensitive (Veh 1,2,3) tumors identified a focal amplification in the region containing Gli2 on Chromosome 1 in 2 out of 3 resistant tumors. Copy number changes are expressed as log2. E, Additional DNA from normal liver (NL), vehicle (controls) and resistant tumors was analyzed by quantitative PCR for the Gli2 locus. F, Correlation between levels of Gli2 mRNA expression and Gli2 copy number is shown for vehicle-treated control tumors (open square) and resistant tumors that emerged after treatment with NVP-LDE225 at 10 bid (green square), 20 qd (red diamond), 40 bid (brown triangle), 80 bid (blue circle) and 160 bid (black inverse triangle) mg/kg/day. Axis in log10 scale. G, Inhibition of Gli2 mRNA levels by siRNA knock-down of Gli2 was associated with decreased proliferation and Gli1 mRNA expression in resistant Gli2 amplified (copy number:20) and Gli2-overexpressing (17-fold) medulloblastoma tumors. Two independent Gli2 siRNAs (Gli2-1 and Gli2-1) were used.

Article Snippet: D , CGH analysis using the Agilent Mouse Genome CGH Microarray Kit 244A of three resistant (LDE 1,2,3) and three sensitive (Veh 1,2,3) tumors identified a focal amplification in the region containing Gli2 on Chromosome 1 in 2 out of 3 resistant tumors.

Techniques: Expressing, Transformation Assay, Microarray, Amplification, Real-time Polymerase Chain Reaction, Inhibition