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A–C. SA β-galactosidase staining performed on wild-type (A), AhCre + Apc fl/fl kidneys with premalignant lesions (B) and tumours from AhCre + Apc fl/fl kidneys (C). Note accumulation of SA β-gal is only observed in the premalignant lesions. Scale bars (A–C) represent 200 µm. D–E. Ki67 IHC showing only a small subset of cell expressing Ki67 in both wt (D) and small lesions from AhCre+ Apcfl/fl mice (E). F. <t>MCM2</t> IHC showing low levels of proliferation in small lesions from AhCre + Apc fl/fl mice, arrows show epithelial cells with low levels of proliferation. (see Supporting Information for pan keratin staining showing the epithelial cells). Scale bars (D–F) represent 20 µm. G. IHC for MCM2 showing that renal carcinomas that grow out from AhCre + Apc fl/fl mice are highly proliferative. Scale bars represent 200 µm. H. Boxplot showing significantly increased Ki67 staining in renal carcinomas compared to very low levels within the premalignant lesions. I–L. IHC showing high levels of β-catenin (I) and p21 (J), but low levels of the proliferation markers Ki67 (K), and MCM2 (L) in small Apc deficient renal lesions. Scale bars (I–L) represent 20 µm.
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A–C. SA β-galactosidase staining performed on wild-type (A), AhCre + Apc fl/fl kidneys with premalignant lesions (B) and tumours from AhCre + Apc fl/fl kidneys (C). Note accumulation of SA β-gal is only observed in the premalignant lesions. Scale bars (A–C) represent 200 µm. D–E. Ki67 IHC showing only a small subset of cell expressing Ki67 in both wt (D) and small lesions from AhCre+ Apcfl/fl mice (E). F. MCM2 IHC showing low levels of proliferation in small lesions from AhCre + Apc fl/fl mice, arrows show epithelial cells with low levels of proliferation. (see Supporting Information for pan keratin staining showing the epithelial cells). Scale bars (D–F) represent 20 µm. G. IHC for MCM2 showing that renal carcinomas that grow out from AhCre + Apc fl/fl mice are highly proliferative. Scale bars represent 200 µm. H. Boxplot showing significantly increased Ki67 staining in renal carcinomas compared to very low levels within the premalignant lesions. I–L. IHC showing high levels of β-catenin (I) and p21 (J), but low levels of the proliferation markers Ki67 (K), and MCM2 (L) in small Apc deficient renal lesions. Scale bars (I–L) represent 20 µm.

Journal: EMBO Molecular Medicine

Article Title: p21 loss blocks senescence following Apc loss and provokes tumourigenesis in the renal but not the intestinal epithelium

doi: 10.1002/emmm.201000101

Figure Lengend Snippet: A–C. SA β-galactosidase staining performed on wild-type (A), AhCre + Apc fl/fl kidneys with premalignant lesions (B) and tumours from AhCre + Apc fl/fl kidneys (C). Note accumulation of SA β-gal is only observed in the premalignant lesions. Scale bars (A–C) represent 200 µm. D–E. Ki67 IHC showing only a small subset of cell expressing Ki67 in both wt (D) and small lesions from AhCre+ Apcfl/fl mice (E). F. MCM2 IHC showing low levels of proliferation in small lesions from AhCre + Apc fl/fl mice, arrows show epithelial cells with low levels of proliferation. (see Supporting Information for pan keratin staining showing the epithelial cells). Scale bars (D–F) represent 20 µm. G. IHC for MCM2 showing that renal carcinomas that grow out from AhCre + Apc fl/fl mice are highly proliferative. Scale bars represent 200 µm. H. Boxplot showing significantly increased Ki67 staining in renal carcinomas compared to very low levels within the premalignant lesions. I–L. IHC showing high levels of β-catenin (I) and p21 (J), but low levels of the proliferation markers Ki67 (K), and MCM2 (L) in small Apc deficient renal lesions. Scale bars (I–L) represent 20 µm.

Article Snippet: Primary antibodies used for immunohistochemistry or immunoflorescence are as follows: p21 (1:500 Santa Cruz, sc471), β-catenin (1:50, Transduction labs, 610154), p16 (1:25, Santa Cruz M-156), SA-β-gal (Senescence β-Galactosidase Staining Kit, Cell signalling pH 5.5), MCM2 (1:200, Cell signalling, 4007), Ki67 (1:250, Labvision, VP-K452), c-myc (1:500, Santa Cruz, N-262, sc764), Keratin (1:50, Thermo scientific, MS-343), CD3 (1:100, Dako, A0452), GFP (1:1000, Abcam ab6556), RFP (1:200, Abcam, ab34771).

Techniques: Staining, Expressing

A. Kaplan–Meier survival graph showing a dramatic acceleration of renal tumourigenesis in AhCre + Apc fl/fl p21 −/− mice (Apc p21 −/− , n = 31, median lifespan 63 days, blue line) compared with AhCre + Apc +/+ (Wt n = 20, <400 days) and AhCre + Apc fl/fl mice (Apc, n = 23, red line, Log rank v Apc fl/fl p21 −/− , p < 0.001). Note there was a marked acceleration of tumourigenesis in AhCre + Apc fl/fl p21 +/− mice (Apc p21 +/− median lifespan 117 days, n = 17, green line, Log rank v Apc fl/fl p < 0.001). B. H&E of a renal tumour in AhCre + Apc fl/fl p21 −/− mice. C–E. Staining shows absence of senescent markers SA β-gal (C), p16 (D) and p21 (E) in AhCre + Apc fl/fl p21 −/− renal tumours. Note there is a small amount non-specific brown staining in the p21 knockout tumours when p21 IHC is performed (black arrow), however all nuclei are blue showing a complete loss of p21 within the tumours (red arrow). F. β-catenin IHC showing continued Wnt signalling activation in AhCre + Apc fl/fl p21 −/− deficient renal tumours. G and H Ki67 IHC (G) and MCM2 IHC (H) showing a marked increase in proliferation in AhCre + Apc fl/fl p21 −/− deficient tumours. Scale bars represent 200 µm.

Journal: EMBO Molecular Medicine

Article Title: p21 loss blocks senescence following Apc loss and provokes tumourigenesis in the renal but not the intestinal epithelium

doi: 10.1002/emmm.201000101

Figure Lengend Snippet: A. Kaplan–Meier survival graph showing a dramatic acceleration of renal tumourigenesis in AhCre + Apc fl/fl p21 −/− mice (Apc p21 −/− , n = 31, median lifespan 63 days, blue line) compared with AhCre + Apc +/+ (Wt n = 20, <400 days) and AhCre + Apc fl/fl mice (Apc, n = 23, red line, Log rank v Apc fl/fl p21 −/− , p < 0.001). Note there was a marked acceleration of tumourigenesis in AhCre + Apc fl/fl p21 +/− mice (Apc p21 +/− median lifespan 117 days, n = 17, green line, Log rank v Apc fl/fl p < 0.001). B. H&E of a renal tumour in AhCre + Apc fl/fl p21 −/− mice. C–E. Staining shows absence of senescent markers SA β-gal (C), p16 (D) and p21 (E) in AhCre + Apc fl/fl p21 −/− renal tumours. Note there is a small amount non-specific brown staining in the p21 knockout tumours when p21 IHC is performed (black arrow), however all nuclei are blue showing a complete loss of p21 within the tumours (red arrow). F. β-catenin IHC showing continued Wnt signalling activation in AhCre + Apc fl/fl p21 −/− deficient renal tumours. G and H Ki67 IHC (G) and MCM2 IHC (H) showing a marked increase in proliferation in AhCre + Apc fl/fl p21 −/− deficient tumours. Scale bars represent 200 µm.

Article Snippet: Primary antibodies used for immunohistochemistry or immunoflorescence are as follows: p21 (1:500 Santa Cruz, sc471), β-catenin (1:50, Transduction labs, 610154), p16 (1:25, Santa Cruz M-156), SA-β-gal (Senescence β-Galactosidase Staining Kit, Cell signalling pH 5.5), MCM2 (1:200, Cell signalling, 4007), Ki67 (1:250, Labvision, VP-K452), c-myc (1:500, Santa Cruz, N-262, sc764), Keratin (1:50, Thermo scientific, MS-343), CD3 (1:100, Dako, A0452), GFP (1:1000, Abcam ab6556), RFP (1:200, Abcam, ab34771).

Techniques: Staining, Knock-Out, Activation Assay

A and B p21 IHC showing a low expression of p21 in a small number of cells in wild-type crypts (labelled Wt) at the crypt villus junction (A), as well as strong upregulation in a subset of cells in the villus following Apc loss in AhCre + Apc fl/fl mice (labelled Apc) (B). C. Apc deficient crypts are not senescent as shown by lack of SA β-gal staining. D and E p16 IHC showing no major upregulation between wt (D) and Apc deficient crypts (E). F and G IHC showing an upregulation of MCM2 staining in the proliferative crypts of Wt mice (F), MCM2 is upregulated in all Apc deficient cells (G). H and I IHC showing an upregulation of Ki67 staining in the proliferative crypts of wt mice (H), Ki67 is upregulated in all Apc deficient cells (I). Scale bars represent 20 µm.

Journal: EMBO Molecular Medicine

Article Title: p21 loss blocks senescence following Apc loss and provokes tumourigenesis in the renal but not the intestinal epithelium

doi: 10.1002/emmm.201000101

Figure Lengend Snippet: A and B p21 IHC showing a low expression of p21 in a small number of cells in wild-type crypts (labelled Wt) at the crypt villus junction (A), as well as strong upregulation in a subset of cells in the villus following Apc loss in AhCre + Apc fl/fl mice (labelled Apc) (B). C. Apc deficient crypts are not senescent as shown by lack of SA β-gal staining. D and E p16 IHC showing no major upregulation between wt (D) and Apc deficient crypts (E). F and G IHC showing an upregulation of MCM2 staining in the proliferative crypts of Wt mice (F), MCM2 is upregulated in all Apc deficient cells (G). H and I IHC showing an upregulation of Ki67 staining in the proliferative crypts of wt mice (H), Ki67 is upregulated in all Apc deficient cells (I). Scale bars represent 20 µm.

Article Snippet: Primary antibodies used for immunohistochemistry or immunoflorescence are as follows: p21 (1:500 Santa Cruz, sc471), β-catenin (1:50, Transduction labs, 610154), p16 (1:25, Santa Cruz M-156), SA-β-gal (Senescence β-Galactosidase Staining Kit, Cell signalling pH 5.5), MCM2 (1:200, Cell signalling, 4007), Ki67 (1:250, Labvision, VP-K452), c-myc (1:500, Santa Cruz, N-262, sc764), Keratin (1:50, Thermo scientific, MS-343), CD3 (1:100, Dako, A0452), GFP (1:1000, Abcam ab6556), RFP (1:200, Abcam, ab34771).

Techniques: Expressing, Staining

A–D. Small intestinal adenomas arising in Apc Min/+ mice at 85 days. IHC showing high levels of β-catenin (A), p21 (B) and Ki67 (C) within adenomas. (D) Intestinal adenomas from Apc Min/+ mice lack expression of senescence marker SA β-gal. E. Apc deficient intestinal lesions that grow out from a non-stem cell ‘hit’ (1.0 mg/kg oral gavage), display high levels of β-catenin (E), with some expression of p21 (F) and high levels of proliferative markers Ki67 (G) and MCM2 (H). I–L. Lgr5-EGFP + - Cre-ER Apc fl/fl mice were treated with a single intraperitoneal injection of tamoxifen to induce recombination in the intestinal stem cell, resulting in intestinal adenoma formation at 24 days. Scale bars (A–H) represent 20 µm. (I) β-catenin IHC showing high levels of expression within intestinal adenomas. J. p21 IHC showing upregulation in intestinal adenomas. K and L IHC showing high levels of proliferation as illustrated by Ki67 (K) and MCM2 (L). Scale bars (I–L) represent 200 µm.

Journal: EMBO Molecular Medicine

Article Title: p21 loss blocks senescence following Apc loss and provokes tumourigenesis in the renal but not the intestinal epithelium

doi: 10.1002/emmm.201000101

Figure Lengend Snippet: A–D. Small intestinal adenomas arising in Apc Min/+ mice at 85 days. IHC showing high levels of β-catenin (A), p21 (B) and Ki67 (C) within adenomas. (D) Intestinal adenomas from Apc Min/+ mice lack expression of senescence marker SA β-gal. E. Apc deficient intestinal lesions that grow out from a non-stem cell ‘hit’ (1.0 mg/kg oral gavage), display high levels of β-catenin (E), with some expression of p21 (F) and high levels of proliferative markers Ki67 (G) and MCM2 (H). I–L. Lgr5-EGFP + - Cre-ER Apc fl/fl mice were treated with a single intraperitoneal injection of tamoxifen to induce recombination in the intestinal stem cell, resulting in intestinal adenoma formation at 24 days. Scale bars (A–H) represent 20 µm. (I) β-catenin IHC showing high levels of expression within intestinal adenomas. J. p21 IHC showing upregulation in intestinal adenomas. K and L IHC showing high levels of proliferation as illustrated by Ki67 (K) and MCM2 (L). Scale bars (I–L) represent 200 µm.

Article Snippet: Primary antibodies used for immunohistochemistry or immunoflorescence are as follows: p21 (1:500 Santa Cruz, sc471), β-catenin (1:50, Transduction labs, 610154), p16 (1:25, Santa Cruz M-156), SA-β-gal (Senescence β-Galactosidase Staining Kit, Cell signalling pH 5.5), MCM2 (1:200, Cell signalling, 4007), Ki67 (1:250, Labvision, VP-K452), c-myc (1:500, Santa Cruz, N-262, sc764), Keratin (1:50, Thermo scientific, MS-343), CD3 (1:100, Dako, A0452), GFP (1:1000, Abcam ab6556), RFP (1:200, Abcam, ab34771).

Techniques: Expressing, Marker, Injection

A. Kaplen–Meier survival graph showing no difference in time to renal tumourigenesis between AhCre + Apc fl/fl p21 −/− (Apc p21, n = 31, black line) and Ah Cre + Apc fl/fl c-Myc fl/fl p21 −/− mice (Apc c-Myc p21 , n = 20, red line) (Log rank p = 0.571), illustrating that c-myc deletion does not affect onset of renal tumourigenesis. B. H&E showing AhCre + Apc fl/fl c-Myc f/fl p21 −/− triple knockout renal tumours. C. Absence of SA β-gal staining in AhCre + Apc fl/fl c-Myc f/fl p21 −/− triple knockout renal tumours. D. β-catenin IHC in AhCre + Apc fl/fl c-Myc f/fl p21 −/− triple knockout renal tumours shows nuclear localization. E. c-Myc IHC showing upregulation of c-Myc in AhCre + Apc fl/fl p21 −/− renal tumours. F. c-Myc IHC shows lack of c-Myc expression in AhCre + Apc fl/fl c-Myc f/fl p21 −/− triple knockout renal tumours, showing c-Myc is not required for tumourigenesis. Scale bars (B–F) represent 200 µm. G and H Strong upregulation of proliferative markers Ki67 (G) and MCM2 (H) showing AhCre + Apc fl/fl c-Myc f/fl p21 −/− triple knockout renal tumours deficient tumours are highly proliferative. Scale bars (G and H) represent 20 µm.

Journal: EMBO Molecular Medicine

Article Title: p21 loss blocks senescence following Apc loss and provokes tumourigenesis in the renal but not the intestinal epithelium

doi: 10.1002/emmm.201000101

Figure Lengend Snippet: A. Kaplen–Meier survival graph showing no difference in time to renal tumourigenesis between AhCre + Apc fl/fl p21 −/− (Apc p21, n = 31, black line) and Ah Cre + Apc fl/fl c-Myc fl/fl p21 −/− mice (Apc c-Myc p21 , n = 20, red line) (Log rank p = 0.571), illustrating that c-myc deletion does not affect onset of renal tumourigenesis. B. H&E showing AhCre + Apc fl/fl c-Myc f/fl p21 −/− triple knockout renal tumours. C. Absence of SA β-gal staining in AhCre + Apc fl/fl c-Myc f/fl p21 −/− triple knockout renal tumours. D. β-catenin IHC in AhCre + Apc fl/fl c-Myc f/fl p21 −/− triple knockout renal tumours shows nuclear localization. E. c-Myc IHC showing upregulation of c-Myc in AhCre + Apc fl/fl p21 −/− renal tumours. F. c-Myc IHC shows lack of c-Myc expression in AhCre + Apc fl/fl c-Myc f/fl p21 −/− triple knockout renal tumours, showing c-Myc is not required for tumourigenesis. Scale bars (B–F) represent 200 µm. G and H Strong upregulation of proliferative markers Ki67 (G) and MCM2 (H) showing AhCre + Apc fl/fl c-Myc f/fl p21 −/− triple knockout renal tumours deficient tumours are highly proliferative. Scale bars (G and H) represent 20 µm.

Article Snippet: Primary antibodies used for immunohistochemistry or immunoflorescence are as follows: p21 (1:500 Santa Cruz, sc471), β-catenin (1:50, Transduction labs, 610154), p16 (1:25, Santa Cruz M-156), SA-β-gal (Senescence β-Galactosidase Staining Kit, Cell signalling pH 5.5), MCM2 (1:200, Cell signalling, 4007), Ki67 (1:250, Labvision, VP-K452), c-myc (1:500, Santa Cruz, N-262, sc764), Keratin (1:50, Thermo scientific, MS-343), CD3 (1:100, Dako, A0452), GFP (1:1000, Abcam ab6556), RFP (1:200, Abcam, ab34771).

Techniques: Triple Knockout, Staining, Expressing