transcriptome analysis console version 4.0.1.36 Search Results


autodock 4.0.1  (AUTODOCK GmbH)
90
AUTODOCK GmbH autodock 4.0.1
Autodock 4.0.1, supplied by AUTODOCK GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/transcriptome+analysis+console+version+4%2E0%2E1%2E36/pmc02724963-135-11-11?v=AUTODOCK+GmbH
Average 90 stars, based on 1 article reviews
autodock 4.0.1 - by Bioz Stars, 2026-08
90/100 stars
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notch2  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology notch2
Figure 2 <t>NOTCH2</t> is a miR-205 target involved in stemness and cancer. (A) Schematic representation of in silico identification of the putative miR-205 targets involved in cell differentiation and cancer. (B) Diagram showing the putative miR-205–targeting seed sequence on NOTCH2–3′ UTR in humans and mice (underline indicates mutation of AAG to CCC in MUT-LUC). (C) Fold change in luciferase activity driven by the WT (WT-LUC) or mutant (MUT-LUC) NOTCH2–3′ UTR reporter under stable expression of miR-205 in BT549 breast cancer cells (n = 3, *P < 0.05). (D) Protein expression of NOTCH2 in MCF12A cells that stably expressed miR-205 or KD miR-205 (sh–miR-205). (E) Protein expression of NOTCH2 in breast cancer cells MDA-MB-231 and BT549 that stably expressed miR-205. (F) miR-205 and NOTCH2 expression levels in the CD44+CD24– stem cells versus the nonstem cells isolated from human PT (n = 3, *P < 0.05). (G) miR-205 and NOTCH2 mRNA expression under 40 μM jag- ged1 treatment in PT cells for 1 day (n = 3, *P < 0.05). Error bars denote mean ± SD.
Notch2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/transcriptome+analysis+console+version+4%2E0%2E1%2E36/10__1172_slash_jci73351-198-38-43?v=Santa+Cruz+Biotechnology
Average 93 stars, based on 1 article reviews
notch2 - by Bioz Stars, 2026-08
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microspectroscopy centre  (Wageningen University and Research)
90
Wageningen University and Research microspectroscopy centre
Figure 2 <t>NOTCH2</t> is a miR-205 target involved in stemness and cancer. (A) Schematic representation of in silico identification of the putative miR-205 targets involved in cell differentiation and cancer. (B) Diagram showing the putative miR-205–targeting seed sequence on NOTCH2–3′ UTR in humans and mice (underline indicates mutation of AAG to CCC in MUT-LUC). (C) Fold change in luciferase activity driven by the WT (WT-LUC) or mutant (MUT-LUC) NOTCH2–3′ UTR reporter under stable expression of miR-205 in BT549 breast cancer cells (n = 3, *P < 0.05). (D) Protein expression of NOTCH2 in MCF12A cells that stably expressed miR-205 or KD miR-205 (sh–miR-205). (E) Protein expression of NOTCH2 in breast cancer cells MDA-MB-231 and BT549 that stably expressed miR-205. (F) miR-205 and NOTCH2 expression levels in the CD44+CD24– stem cells versus the nonstem cells isolated from human PT (n = 3, *P < 0.05). (G) miR-205 and NOTCH2 mRNA expression under 40 μM jag- ged1 treatment in PT cells for 1 day (n = 3, *P < 0.05). Error bars denote mean ± SD.
Microspectroscopy Centre, supplied by Wageningen University and Research, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/transcriptome+analysis+console+version+4%2E0%2E1%2E36/pm28116374-22-26-30?v=Wageningen+University+and+Research
Average 90 stars, based on 1 article reviews
microspectroscopy centre - by Bioz Stars, 2026-08
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µct scanner  (SCANCO USA INC)
90
SCANCO USA INC µct scanner
Figure 2 <t>NOTCH2</t> is a miR-205 target involved in stemness and cancer. (A) Schematic representation of in silico identification of the putative miR-205 targets involved in cell differentiation and cancer. (B) Diagram showing the putative miR-205–targeting seed sequence on NOTCH2–3′ UTR in humans and mice (underline indicates mutation of AAG to CCC in MUT-LUC). (C) Fold change in luciferase activity driven by the WT (WT-LUC) or mutant (MUT-LUC) NOTCH2–3′ UTR reporter under stable expression of miR-205 in BT549 breast cancer cells (n = 3, *P < 0.05). (D) Protein expression of NOTCH2 in MCF12A cells that stably expressed miR-205 or KD miR-205 (sh–miR-205). (E) Protein expression of NOTCH2 in breast cancer cells MDA-MB-231 and BT549 that stably expressed miR-205. (F) miR-205 and NOTCH2 expression levels in the CD44+CD24– stem cells versus the nonstem cells isolated from human PT (n = 3, *P < 0.05). (G) miR-205 and NOTCH2 mRNA expression under 40 μM jag- ged1 treatment in PT cells for 1 day (n = 3, *P < 0.05). Error bars denote mean ± SD.
µct Scanner, supplied by SCANCO USA INC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/transcriptome+analysis+console+version+4%2E0%2E1%2E36/10__1530_slash_joe___18___0244-51-23-26?v=SCANCO+USA+INC
Average 90 stars, based on 1 article reviews
µct scanner - by Bioz Stars, 2026-08
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dsm 40136  (DSMZ)
92
DSMZ dsm 40136
Figure 2 <t>NOTCH2</t> is a miR-205 target involved in stemness and cancer. (A) Schematic representation of in silico identification of the putative miR-205 targets involved in cell differentiation and cancer. (B) Diagram showing the putative miR-205–targeting seed sequence on NOTCH2–3′ UTR in humans and mice (underline indicates mutation of AAG to CCC in MUT-LUC). (C) Fold change in luciferase activity driven by the WT (WT-LUC) or mutant (MUT-LUC) NOTCH2–3′ UTR reporter under stable expression of miR-205 in BT549 breast cancer cells (n = 3, *P < 0.05). (D) Protein expression of NOTCH2 in MCF12A cells that stably expressed miR-205 or KD miR-205 (sh–miR-205). (E) Protein expression of NOTCH2 in breast cancer cells MDA-MB-231 and BT549 that stably expressed miR-205. (F) miR-205 and NOTCH2 expression levels in the CD44+CD24– stem cells versus the nonstem cells isolated from human PT (n = 3, *P < 0.05). (G) miR-205 and NOTCH2 mRNA expression under 40 μM jag- ged1 treatment in PT cells for 1 day (n = 3, *P < 0.05). Error bars denote mean ± SD.
Dsm 40136, supplied by DSMZ, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/transcriptome+analysis+console+version+4%2E0%2E1%2E36/ppr0557606-149-175-179?v=DSMZ
Average 92 stars, based on 1 article reviews
dsm 40136 - by Bioz Stars, 2026-08
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trans 4  (Chem Impex International)
95
Chem Impex International trans 4
Figure 2 <t>NOTCH2</t> is a miR-205 target involved in stemness and cancer. (A) Schematic representation of in silico identification of the putative miR-205 targets involved in cell differentiation and cancer. (B) Diagram showing the putative miR-205–targeting seed sequence on NOTCH2–3′ UTR in humans and mice (underline indicates mutation of AAG to CCC in MUT-LUC). (C) Fold change in luciferase activity driven by the WT (WT-LUC) or mutant (MUT-LUC) NOTCH2–3′ UTR reporter under stable expression of miR-205 in BT549 breast cancer cells (n = 3, *P < 0.05). (D) Protein expression of NOTCH2 in MCF12A cells that stably expressed miR-205 or KD miR-205 (sh–miR-205). (E) Protein expression of NOTCH2 in breast cancer cells MDA-MB-231 and BT549 that stably expressed miR-205. (F) miR-205 and NOTCH2 expression levels in the CD44+CD24– stem cells versus the nonstem cells isolated from human PT (n = 3, *P < 0.05). (G) miR-205 and NOTCH2 mRNA expression under 40 μM jag- ged1 treatment in PT cells for 1 day (n = 3, *P < 0.05). Error bars denote mean ± SD.
Trans 4, supplied by Chem Impex International, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/transcriptome+analysis+console+version+4%2E0%2E1%2E36/us10005788-831-10-13?v=Chem+Impex+International
Average 95 stars, based on 1 article reviews
trans 4 - by Bioz Stars, 2026-08
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Image Search Results


Figure 2 NOTCH2 is a miR-205 target involved in stemness and cancer. (A) Schematic representation of in silico identification of the putative miR-205 targets involved in cell differentiation and cancer. (B) Diagram showing the putative miR-205–targeting seed sequence on NOTCH2–3′ UTR in humans and mice (underline indicates mutation of AAG to CCC in MUT-LUC). (C) Fold change in luciferase activity driven by the WT (WT-LUC) or mutant (MUT-LUC) NOTCH2–3′ UTR reporter under stable expression of miR-205 in BT549 breast cancer cells (n = 3, *P < 0.05). (D) Protein expression of NOTCH2 in MCF12A cells that stably expressed miR-205 or KD miR-205 (sh–miR-205). (E) Protein expression of NOTCH2 in breast cancer cells MDA-MB-231 and BT549 that stably expressed miR-205. (F) miR-205 and NOTCH2 expression levels in the CD44+CD24– stem cells versus the nonstem cells isolated from human PT (n = 3, *P < 0.05). (G) miR-205 and NOTCH2 mRNA expression under 40 μM jag- ged1 treatment in PT cells for 1 day (n = 3, *P < 0.05). Error bars denote mean ± SD.

Journal: Journal of Clinical Investigation

Article Title: MicroRNA-205 signaling regulates mammary stem cell fate and tumorigenesis

doi: 10.1172/jci73351

Figure Lengend Snippet: Figure 2 NOTCH2 is a miR-205 target involved in stemness and cancer. (A) Schematic representation of in silico identification of the putative miR-205 targets involved in cell differentiation and cancer. (B) Diagram showing the putative miR-205–targeting seed sequence on NOTCH2–3′ UTR in humans and mice (underline indicates mutation of AAG to CCC in MUT-LUC). (C) Fold change in luciferase activity driven by the WT (WT-LUC) or mutant (MUT-LUC) NOTCH2–3′ UTR reporter under stable expression of miR-205 in BT549 breast cancer cells (n = 3, *P < 0.05). (D) Protein expression of NOTCH2 in MCF12A cells that stably expressed miR-205 or KD miR-205 (sh–miR-205). (E) Protein expression of NOTCH2 in breast cancer cells MDA-MB-231 and BT549 that stably expressed miR-205. (F) miR-205 and NOTCH2 expression levels in the CD44+CD24– stem cells versus the nonstem cells isolated from human PT (n = 3, *P < 0.05). (G) miR-205 and NOTCH2 mRNA expression under 40 μM jag- ged1 treatment in PT cells for 1 day (n = 3, *P < 0.05). Error bars denote mean ± SD.

Article Snippet: For the NOTCH inhibitor GSI treatment, 5 μM γ-Secretase Inhibitor IX (DAPT, N-[N-(3,5-Difluorophenacetyl-L-alanyl)]-S-phenylglycine-t-Butyl Ester; EMD Millipore) or DMSO was used. miR-205 precursor, miR-205 antagomir, and negative control oligos (50 nmole) were purchased from Ambion. siRNAs (200 pmole) targeting NOTCH2 and ZEB1 were from Santa Cruz Biotechnology Inc. Transfection of miR-205 oligos as well as the above siRNAs was performed by Lipofectamine 2000 following the manufacturer’s instructions.

Techniques: In Silico, Cell Differentiation, Sequencing, Mutagenesis, Luciferase, Activity Assay, Expressing, Stable Transfection, Isolation

Figure 3 miR-205 regulates stem cell properties through downregulation of NOTCH2. (A) The percentage of the CD24–CD44+ population (left) and NOTCH2 protein expression (right) in sh-Vec and sh–miR-205–MCF12A cells transfected with NOTCH2 siRNA (n = 3, *P < 0.05; **P < 0.01; sc, scrambled control siRNA). (B) Expression levels of miR-205 and NOTCH2 mRNA in sh-Vec and sh–miR-205–MCF12A cells transfected with NOTCH2 siRNA (n = 3, *P < 0.05; **P < 0.01). Error bars denote mean ± SD. (C) The percentage of CD24–CD44+ population in MB-MDA-231, BT549, and PT cells that stably expressed miR-205 (n = 3, *P < 0.05). (D) The percentage of CD24–CD44+ population in BT549 and PT cells transfected with NOTCH2 siRNA or (E) treated with 5 μM of GSI for 4 days (n = 3, *P < 0.05).

Journal: Journal of Clinical Investigation

Article Title: MicroRNA-205 signaling regulates mammary stem cell fate and tumorigenesis

doi: 10.1172/jci73351

Figure Lengend Snippet: Figure 3 miR-205 regulates stem cell properties through downregulation of NOTCH2. (A) The percentage of the CD24–CD44+ population (left) and NOTCH2 protein expression (right) in sh-Vec and sh–miR-205–MCF12A cells transfected with NOTCH2 siRNA (n = 3, *P < 0.05; **P < 0.01; sc, scrambled control siRNA). (B) Expression levels of miR-205 and NOTCH2 mRNA in sh-Vec and sh–miR-205–MCF12A cells transfected with NOTCH2 siRNA (n = 3, *P < 0.05; **P < 0.01). Error bars denote mean ± SD. (C) The percentage of CD24–CD44+ population in MB-MDA-231, BT549, and PT cells that stably expressed miR-205 (n = 3, *P < 0.05). (D) The percentage of CD24–CD44+ population in BT549 and PT cells transfected with NOTCH2 siRNA or (E) treated with 5 μM of GSI for 4 days (n = 3, *P < 0.05).

Article Snippet: For the NOTCH inhibitor GSI treatment, 5 μM γ-Secretase Inhibitor IX (DAPT, N-[N-(3,5-Difluorophenacetyl-L-alanyl)]-S-phenylglycine-t-Butyl Ester; EMD Millipore) or DMSO was used. miR-205 precursor, miR-205 antagomir, and negative control oligos (50 nmole) were purchased from Ambion. siRNAs (200 pmole) targeting NOTCH2 and ZEB1 were from Santa Cruz Biotechnology Inc. Transfection of miR-205 oligos as well as the above siRNAs was performed by Lipofectamine 2000 following the manufacturer’s instructions.

Techniques: Expressing, Transfection, Control, Stable Transfection

Figure 5 Loss of miR-205 promotes self-renewing, symmetrically dividing stem cell population through coordinated activation of NOTCH2 and ZEB1. (A) The percentage of the symmetric and asymmetric cell division patterns in the isolated CD44hi-MCF12A cells expressing control sh-Vec and sh–miR-205 along with NOTCH2 or ZEB1 siRNA (n = 3, 70–110 cells were counted per sample, *P < 0.05). Protein expression levels of (B) NOTCH2 and (C) ZEB1 in the isolated CD44hi population expressing the indicated constructs. (D) mRNA expression of stemness-related genes in MCF12A cells expressing sh-Vec, sh–miR-205, or sh–miR-205 with NOTCH2 siRNA (n = 3, *P < 0.05). (E) mRNA expression of polarity genes in MCF12A cells expressing sh-Vec, sh–miR-205, or sh–miR-205 with ZEB1 siRNA (n = 3, *P < 0.05). (F) Number of forming spheres per 1,000 cells generated from MCF12A cells expressing sh-Vec, sh–miR-205, sh–miR-205 with NOTCH2 siRNA, or sh–miR-205 with ZEB1 siRNA for 3 serial passages (n = 3, *P < 0.05 compared with primary sphere in each group). Error bars denote mean ± SD.

Journal: Journal of Clinical Investigation

Article Title: MicroRNA-205 signaling regulates mammary stem cell fate and tumorigenesis

doi: 10.1172/jci73351

Figure Lengend Snippet: Figure 5 Loss of miR-205 promotes self-renewing, symmetrically dividing stem cell population through coordinated activation of NOTCH2 and ZEB1. (A) The percentage of the symmetric and asymmetric cell division patterns in the isolated CD44hi-MCF12A cells expressing control sh-Vec and sh–miR-205 along with NOTCH2 or ZEB1 siRNA (n = 3, 70–110 cells were counted per sample, *P < 0.05). Protein expression levels of (B) NOTCH2 and (C) ZEB1 in the isolated CD44hi population expressing the indicated constructs. (D) mRNA expression of stemness-related genes in MCF12A cells expressing sh-Vec, sh–miR-205, or sh–miR-205 with NOTCH2 siRNA (n = 3, *P < 0.05). (E) mRNA expression of polarity genes in MCF12A cells expressing sh-Vec, sh–miR-205, or sh–miR-205 with ZEB1 siRNA (n = 3, *P < 0.05). (F) Number of forming spheres per 1,000 cells generated from MCF12A cells expressing sh-Vec, sh–miR-205, sh–miR-205 with NOTCH2 siRNA, or sh–miR-205 with ZEB1 siRNA for 3 serial passages (n = 3, *P < 0.05 compared with primary sphere in each group). Error bars denote mean ± SD.

Article Snippet: For the NOTCH inhibitor GSI treatment, 5 μM γ-Secretase Inhibitor IX (DAPT, N-[N-(3,5-Difluorophenacetyl-L-alanyl)]-S-phenylglycine-t-Butyl Ester; EMD Millipore) or DMSO was used. miR-205 precursor, miR-205 antagomir, and negative control oligos (50 nmole) were purchased from Ambion. siRNAs (200 pmole) targeting NOTCH2 and ZEB1 were from Santa Cruz Biotechnology Inc. Transfection of miR-205 oligos as well as the above siRNAs was performed by Lipofectamine 2000 following the manufacturer’s instructions.

Techniques: Activation Assay, Isolation, Expressing, Control, Construct, Generated

Figure 7 Loss of miR-205 is positively correlated with enhanced expression levels of NOTCH2 and ZEB1 in aggressive human breast tumors. (A) Rep- resentative cases from 98 breast cancer specimens in tissue microarrays were analyzed by immunohistochemical staining (NOTCH2) and by in situ hybridization (miR-205). Scale bars: 100 μm. (B) Representative images showing a reverse correlation of miR-205 with NOTCH2, ZEB1, and JAG1 expression. Scale bars: 100 μm.

Journal: Journal of Clinical Investigation

Article Title: MicroRNA-205 signaling regulates mammary stem cell fate and tumorigenesis

doi: 10.1172/jci73351

Figure Lengend Snippet: Figure 7 Loss of miR-205 is positively correlated with enhanced expression levels of NOTCH2 and ZEB1 in aggressive human breast tumors. (A) Rep- resentative cases from 98 breast cancer specimens in tissue microarrays were analyzed by immunohistochemical staining (NOTCH2) and by in situ hybridization (miR-205). Scale bars: 100 μm. (B) Representative images showing a reverse correlation of miR-205 with NOTCH2, ZEB1, and JAG1 expression. Scale bars: 100 μm.

Article Snippet: For the NOTCH inhibitor GSI treatment, 5 μM γ-Secretase Inhibitor IX (DAPT, N-[N-(3,5-Difluorophenacetyl-L-alanyl)]-S-phenylglycine-t-Butyl Ester; EMD Millipore) or DMSO was used. miR-205 precursor, miR-205 antagomir, and negative control oligos (50 nmole) were purchased from Ambion. siRNAs (200 pmole) targeting NOTCH2 and ZEB1 were from Santa Cruz Biotechnology Inc. Transfection of miR-205 oligos as well as the above siRNAs was performed by Lipofectamine 2000 following the manufacturer’s instructions.

Techniques: Expressing, Immunohistochemical staining, Staining, In Situ Hybridization

Figure 8 miR-205 coordinately regulates NOTCH2 and ZEB1 to control stem cell self renewal and SD. (A and B) A proposed model illustrating that jagged1-NOTCH signaling downregulates miR-205 and loss of miR-205 promotes self renewal and SD through constitutive activation of NOTCH2 and ZEB1, leading to expansion of stem cell and tumor stem cell populations.

Journal: Journal of Clinical Investigation

Article Title: MicroRNA-205 signaling regulates mammary stem cell fate and tumorigenesis

doi: 10.1172/jci73351

Figure Lengend Snippet: Figure 8 miR-205 coordinately regulates NOTCH2 and ZEB1 to control stem cell self renewal and SD. (A and B) A proposed model illustrating that jagged1-NOTCH signaling downregulates miR-205 and loss of miR-205 promotes self renewal and SD through constitutive activation of NOTCH2 and ZEB1, leading to expansion of stem cell and tumor stem cell populations.

Article Snippet: For the NOTCH inhibitor GSI treatment, 5 μM γ-Secretase Inhibitor IX (DAPT, N-[N-(3,5-Difluorophenacetyl-L-alanyl)]-S-phenylglycine-t-Butyl Ester; EMD Millipore) or DMSO was used. miR-205 precursor, miR-205 antagomir, and negative control oligos (50 nmole) were purchased from Ambion. siRNAs (200 pmole) targeting NOTCH2 and ZEB1 were from Santa Cruz Biotechnology Inc. Transfection of miR-205 oligos as well as the above siRNAs was performed by Lipofectamine 2000 following the manufacturer’s instructions.

Techniques: Control, Activation Assay