mouse anti 295 cdk2 Search Results


mouse anti 295 cdk2  (Santa Cruz Biotechnology)
96
Santa Cruz Biotechnology mouse anti 295 cdk2
Mouse Anti 295 Cdk2, supplied by Santa Cruz Biotechnology, 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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Average 96 stars, based on 1 article reviews
mouse anti 295 cdk2 - by Bioz Stars, 2026-03
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anti cdk 2  (Boster Bio)
93
Boster Bio anti cdk 2
Anti Cdk 2, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti cdk 2 - by Bioz Stars, 2026-03
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anti cdk 2 boster  (Proteintech)
96
Proteintech anti cdk 2 boster
Anti Cdk 2 Boster, supplied by Proteintech, 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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anti cdk 2 boster - by Bioz Stars, 2026-03
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anti cdk 2  (Cell Signaling Technology Inc)
95
Cell Signaling Technology Inc anti cdk 2
Anti Cdk 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti cdk 2 - by Bioz Stars, 2026-03
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cdk 2  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc cdk 2
A working model of the synergistic effect of ADT‐OH and celecoxib on colorectal cancer HCT116 cells. In HCT116 cells, the combination of ADT‐OH and celecoxib inhibited cell migration by downregulating the expressions of LIMK, cofilin, MMP2, and MMP9. Furthermore, the combination of ADT‐OH and celecoxib resulted in cell cycle arrest in the G2/M phase by upregulating p21 expression and <t>downregulating</t> <t>CDK2</t> and cyclin D1 expression. Meanwhile, the combination of ADT‐OH and celecoxib promoted the production of reactive oxygen species in HCT116 cells, which in turn led to the accumulation of intracellular MDA and the decrease of SOD. Furthermore, the combination of ADT‐OH and celecoxib induced apoptosis by upregulating cleaved caspase 3 and Bax expression and downregulating Bcl‐2 expression. All the above may explain the synergistic effect of ADT‐OH and celecoxib in inhibiting the growth of HCT116 cells.
Cdk 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/cdk 2/product/Cell Signaling Technology Inc
Average 96 stars, based on 1 article reviews
cdk 2 - by Bioz Stars, 2026-03
96/100 stars
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anti-histone  (GenScript corporation)
90
GenScript corporation anti-histone
A working model of the synergistic effect of ADT‐OH and celecoxib on colorectal cancer HCT116 cells. In HCT116 cells, the combination of ADT‐OH and celecoxib inhibited cell migration by downregulating the expressions of LIMK, cofilin, MMP2, and MMP9. Furthermore, the combination of ADT‐OH and celecoxib resulted in cell cycle arrest in the G2/M phase by upregulating p21 expression and <t>downregulating</t> <t>CDK2</t> and cyclin D1 expression. Meanwhile, the combination of ADT‐OH and celecoxib promoted the production of reactive oxygen species in HCT116 cells, which in turn led to the accumulation of intracellular MDA and the decrease of SOD. Furthermore, the combination of ADT‐OH and celecoxib induced apoptosis by upregulating cleaved caspase 3 and Bax expression and downregulating Bcl‐2 expression. All the above may explain the synergistic effect of ADT‐OH and celecoxib in inhibiting the growth of HCT116 cells.
Anti Histone, supplied by GenScript corporation, 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/result/anti-histone/product/GenScript corporation
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m00166-3  (Boster Bio)
90
Boster Bio m00166-3
A working model of the synergistic effect of ADT‐OH and celecoxib on colorectal cancer HCT116 cells. In HCT116 cells, the combination of ADT‐OH and celecoxib inhibited cell migration by downregulating the expressions of LIMK, cofilin, MMP2, and MMP9. Furthermore, the combination of ADT‐OH and celecoxib resulted in cell cycle arrest in the G2/M phase by upregulating p21 expression and <t>downregulating</t> <t>CDK2</t> and cyclin D1 expression. Meanwhile, the combination of ADT‐OH and celecoxib promoted the production of reactive oxygen species in HCT116 cells, which in turn led to the accumulation of intracellular MDA and the decrease of SOD. Furthermore, the combination of ADT‐OH and celecoxib induced apoptosis by upregulating cleaved caspase 3 and Bax expression and downregulating Bcl‐2 expression. All the above may explain the synergistic effect of ADT‐OH and celecoxib in inhibiting the growth of HCT116 cells.
M00166 3, supplied by Boster Bio, 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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m00166-3 - by Bioz Stars, 2026-03
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anti-cdk 2 t160  (Cell Signaling Technology Inc)
90
Cell Signaling Technology Inc anti-cdk 2 t160
A working model of the synergistic effect of ADT‐OH and celecoxib on colorectal cancer HCT116 cells. In HCT116 cells, the combination of ADT‐OH and celecoxib inhibited cell migration by downregulating the expressions of LIMK, cofilin, MMP2, and MMP9. Furthermore, the combination of ADT‐OH and celecoxib resulted in cell cycle arrest in the G2/M phase by upregulating p21 expression and <t>downregulating</t> <t>CDK2</t> and cyclin D1 expression. Meanwhile, the combination of ADT‐OH and celecoxib promoted the production of reactive oxygen species in HCT116 cells, which in turn led to the accumulation of intracellular MDA and the decrease of SOD. Furthermore, the combination of ADT‐OH and celecoxib induced apoptosis by upregulating cleaved caspase 3 and Bax expression and downregulating Bcl‐2 expression. All the above may explain the synergistic effect of ADT‐OH and celecoxib in inhibiting the growth of HCT116 cells.
Anti Cdk 2 T160, supplied by Cell Signaling Technology 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/result/anti-cdk 2 t160/product/Cell Signaling Technology Inc
Average 90 stars, based on 1 article reviews
anti-cdk 2 t160 - by Bioz Stars, 2026-03
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anti-cdk 2  (Boster Bio)
90
Boster Bio anti-cdk 2
A working model of the synergistic effect of ADT‐OH and celecoxib on colorectal cancer HCT116 cells. In HCT116 cells, the combination of ADT‐OH and celecoxib inhibited cell migration by downregulating the expressions of LIMK, cofilin, MMP2, and MMP9. Furthermore, the combination of ADT‐OH and celecoxib resulted in cell cycle arrest in the G2/M phase by upregulating p21 expression and <t>downregulating</t> <t>CDK2</t> and cyclin D1 expression. Meanwhile, the combination of ADT‐OH and celecoxib promoted the production of reactive oxygen species in HCT116 cells, which in turn led to the accumulation of intracellular MDA and the decrease of SOD. Furthermore, the combination of ADT‐OH and celecoxib induced apoptosis by upregulating cleaved caspase 3 and Bax expression and downregulating Bcl‐2 expression. All the above may explain the synergistic effect of ADT‐OH and celecoxib in inhibiting the growth of HCT116 cells.
Anti Cdk 2, supplied by Boster Bio, 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/result/anti-cdk 2/product/Boster Bio
Average 90 stars, based on 1 article reviews
anti-cdk 2 - by Bioz Stars, 2026-03
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Image Search Results


A working model of the synergistic effect of ADT‐OH and celecoxib on colorectal cancer HCT116 cells. In HCT116 cells, the combination of ADT‐OH and celecoxib inhibited cell migration by downregulating the expressions of LIMK, cofilin, MMP2, and MMP9. Furthermore, the combination of ADT‐OH and celecoxib resulted in cell cycle arrest in the G2/M phase by upregulating p21 expression and downregulating CDK2 and cyclin D1 expression. Meanwhile, the combination of ADT‐OH and celecoxib promoted the production of reactive oxygen species in HCT116 cells, which in turn led to the accumulation of intracellular MDA and the decrease of SOD. Furthermore, the combination of ADT‐OH and celecoxib induced apoptosis by upregulating cleaved caspase 3 and Bax expression and downregulating Bcl‐2 expression. All the above may explain the synergistic effect of ADT‐OH and celecoxib in inhibiting the growth of HCT116 cells.

Journal: Cancer Medicine

Article Title: ADT‐OH synergistically enhanced the antitumor activity of celecoxib in human colorectal cancer cells

doi: 10.1002/cam4.6342

Figure Lengend Snippet: A working model of the synergistic effect of ADT‐OH and celecoxib on colorectal cancer HCT116 cells. In HCT116 cells, the combination of ADT‐OH and celecoxib inhibited cell migration by downregulating the expressions of LIMK, cofilin, MMP2, and MMP9. Furthermore, the combination of ADT‐OH and celecoxib resulted in cell cycle arrest in the G2/M phase by upregulating p21 expression and downregulating CDK2 and cyclin D1 expression. Meanwhile, the combination of ADT‐OH and celecoxib promoted the production of reactive oxygen species in HCT116 cells, which in turn led to the accumulation of intracellular MDA and the decrease of SOD. Furthermore, the combination of ADT‐OH and celecoxib induced apoptosis by upregulating cleaved caspase 3 and Bax expression and downregulating Bcl‐2 expression. All the above may explain the synergistic effect of ADT‐OH and celecoxib in inhibiting the growth of HCT116 cells.

Article Snippet: CDK‐2 , 18,048 , Cell Signaling Technology.

Techniques: Migration, Expressing