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map4k4  (MedChemExpress)


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    MedChemExpress map4k4
    Interfering Notch and <t>MAP4K4</t> signaling pathways in OC cells. Panel A: combination treatment of cisplatin and GSIs. SKOV3 CP cells were treated under the following conditions: ( A ) medium control, ( B ) 2 µg/ml cisplatin, ( C ) 2 µg/ml cisplatin + 5 µM DAPT, and ( D ) 2 µg/ml cisplatin + 1 µM RG-4733 for 120 h. The simultaneous administration of cisplatin and GSIs did not reverse the neuronal morphology of SKOV3 CP cells ( A - D ). Additionally, this combination did not lead to significant changes in Notch3 expression ( E ). However, the incubation with both GSIs induced an upregulation of PAX6 and ChgA, with RG-4733 exerting the most pronounced effect. Panel B : combination treatment of MAP4K4i and GSIs in OC Cells. The exposure of OC cells to MAP4K4i did not induce general changes as expected in HES1 protein levels across various OC cell lines. However, both GSIs significantly downregulated HES1 protein expression ( A - D ). Notch3 expression was stimulated by all inhibitors in both SKOV3 WT and SKOV3 CP cells ( E ). In OVCAR-3 and primary OC cells OC236, only the combination of MAP4K4i with RG-4733 synergistically enhanced Notch3 expression ( G - H ). Furthermore, βIII-tubulin expression was strongly stimulated by the MAP4K4i in SKOV3 WT cells, an effect not observed in the resistant SKOV3 CP subline. Nevertheless, the combination of MAP4K4i with GSIs led to an enhanced expression of this neuronal-related structural protein ( I - J ). ChgA expression was slightly repressed in SKOV3 WT cells but enhanced in SKOV3 CP cells after 24 h of MAP4K4 inhibitor treatment. Both GSIs increased ChgA expression, and this effect was slightly potentiated in the presence of the MAP4K4 inhibitor ( K - L ). Abbreviations: M : MAP4K4i; D : DAPT; RG : RG-4733; AU : arbitrary units. Bar graphs represent densitometric analyses of western blots performed to measure protein expression following drug exposure. Results are representative of n = 3 independent experiments.
    Map4k4, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 92/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "The neuroepithelial origin of ovarian carcinomas explained through an epithelial-mesenchymal-ectodermal transition enhanced by cisplatin"

    Article Title: The neuroepithelial origin of ovarian carcinomas explained through an epithelial-mesenchymal-ectodermal transition enhanced by cisplatin

    Journal: Scientific Reports

    doi: 10.1038/s41598-024-76984-9

    Interfering Notch and MAP4K4 signaling pathways in OC cells. Panel A: combination treatment of cisplatin and GSIs. SKOV3 CP cells were treated under the following conditions: ( A ) medium control, ( B ) 2 µg/ml cisplatin, ( C ) 2 µg/ml cisplatin + 5 µM DAPT, and ( D ) 2 µg/ml cisplatin + 1 µM RG-4733 for 120 h. The simultaneous administration of cisplatin and GSIs did not reverse the neuronal morphology of SKOV3 CP cells ( A - D ). Additionally, this combination did not lead to significant changes in Notch3 expression ( E ). However, the incubation with both GSIs induced an upregulation of PAX6 and ChgA, with RG-4733 exerting the most pronounced effect. Panel B : combination treatment of MAP4K4i and GSIs in OC Cells. The exposure of OC cells to MAP4K4i did not induce general changes as expected in HES1 protein levels across various OC cell lines. However, both GSIs significantly downregulated HES1 protein expression ( A - D ). Notch3 expression was stimulated by all inhibitors in both SKOV3 WT and SKOV3 CP cells ( E ). In OVCAR-3 and primary OC cells OC236, only the combination of MAP4K4i with RG-4733 synergistically enhanced Notch3 expression ( G - H ). Furthermore, βIII-tubulin expression was strongly stimulated by the MAP4K4i in SKOV3 WT cells, an effect not observed in the resistant SKOV3 CP subline. Nevertheless, the combination of MAP4K4i with GSIs led to an enhanced expression of this neuronal-related structural protein ( I - J ). ChgA expression was slightly repressed in SKOV3 WT cells but enhanced in SKOV3 CP cells after 24 h of MAP4K4 inhibitor treatment. Both GSIs increased ChgA expression, and this effect was slightly potentiated in the presence of the MAP4K4 inhibitor ( K - L ). Abbreviations: M : MAP4K4i; D : DAPT; RG : RG-4733; AU : arbitrary units. Bar graphs represent densitometric analyses of western blots performed to measure protein expression following drug exposure. Results are representative of n = 3 independent experiments.
    Figure Legend Snippet: Interfering Notch and MAP4K4 signaling pathways in OC cells. Panel A: combination treatment of cisplatin and GSIs. SKOV3 CP cells were treated under the following conditions: ( A ) medium control, ( B ) 2 µg/ml cisplatin, ( C ) 2 µg/ml cisplatin + 5 µM DAPT, and ( D ) 2 µg/ml cisplatin + 1 µM RG-4733 for 120 h. The simultaneous administration of cisplatin and GSIs did not reverse the neuronal morphology of SKOV3 CP cells ( A - D ). Additionally, this combination did not lead to significant changes in Notch3 expression ( E ). However, the incubation with both GSIs induced an upregulation of PAX6 and ChgA, with RG-4733 exerting the most pronounced effect. Panel B : combination treatment of MAP4K4i and GSIs in OC Cells. The exposure of OC cells to MAP4K4i did not induce general changes as expected in HES1 protein levels across various OC cell lines. However, both GSIs significantly downregulated HES1 protein expression ( A - D ). Notch3 expression was stimulated by all inhibitors in both SKOV3 WT and SKOV3 CP cells ( E ). In OVCAR-3 and primary OC cells OC236, only the combination of MAP4K4i with RG-4733 synergistically enhanced Notch3 expression ( G - H ). Furthermore, βIII-tubulin expression was strongly stimulated by the MAP4K4i in SKOV3 WT cells, an effect not observed in the resistant SKOV3 CP subline. Nevertheless, the combination of MAP4K4i with GSIs led to an enhanced expression of this neuronal-related structural protein ( I - J ). ChgA expression was slightly repressed in SKOV3 WT cells but enhanced in SKOV3 CP cells after 24 h of MAP4K4 inhibitor treatment. Both GSIs increased ChgA expression, and this effect was slightly potentiated in the presence of the MAP4K4 inhibitor ( K - L ). Abbreviations: M : MAP4K4i; D : DAPT; RG : RG-4733; AU : arbitrary units. Bar graphs represent densitometric analyses of western blots performed to measure protein expression following drug exposure. Results are representative of n = 3 independent experiments.

    Techniques Used: Protein-Protein interactions, Control, Expressing, Incubation, Western Blot



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    Interfering Notch and <t>MAP4K4</t> signaling pathways in OC cells. Panel A: combination treatment of cisplatin and GSIs. SKOV3 CP cells were treated under the following conditions: ( A ) medium control, ( B ) 2 µg/ml cisplatin, ( C ) 2 µg/ml cisplatin + 5 µM DAPT, and ( D ) 2 µg/ml cisplatin + 1 µM RG-4733 for 120 h. The simultaneous administration of cisplatin and GSIs did not reverse the neuronal morphology of SKOV3 CP cells ( A - D ). Additionally, this combination did not lead to significant changes in Notch3 expression ( E ). However, the incubation with both GSIs induced an upregulation of PAX6 and ChgA, with RG-4733 exerting the most pronounced effect. Panel B : combination treatment of MAP4K4i and GSIs in OC Cells. The exposure of OC cells to MAP4K4i did not induce general changes as expected in HES1 protein levels across various OC cell lines. However, both GSIs significantly downregulated HES1 protein expression ( A - D ). Notch3 expression was stimulated by all inhibitors in both SKOV3 WT and SKOV3 CP cells ( E ). In OVCAR-3 and primary OC cells OC236, only the combination of MAP4K4i with RG-4733 synergistically enhanced Notch3 expression ( G - H ). Furthermore, βIII-tubulin expression was strongly stimulated by the MAP4K4i in SKOV3 WT cells, an effect not observed in the resistant SKOV3 CP subline. Nevertheless, the combination of MAP4K4i with GSIs led to an enhanced expression of this neuronal-related structural protein ( I - J ). ChgA expression was slightly repressed in SKOV3 WT cells but enhanced in SKOV3 CP cells after 24 h of MAP4K4 inhibitor treatment. Both GSIs increased ChgA expression, and this effect was slightly potentiated in the presence of the MAP4K4 inhibitor ( K - L ). Abbreviations: M : MAP4K4i; D : DAPT; RG : RG-4733; AU : arbitrary units. Bar graphs represent densitometric analyses of western blots performed to measure protein expression following drug exposure. Results are representative of n = 3 independent experiments.
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    Interfering Notch and <t>MAP4K4</t> signaling pathways in OC cells. Panel A: combination treatment of cisplatin and GSIs. SKOV3 CP cells were treated under the following conditions: ( A ) medium control, ( B ) 2 µg/ml cisplatin, ( C ) 2 µg/ml cisplatin + 5 µM DAPT, and ( D ) 2 µg/ml cisplatin + 1 µM RG-4733 for 120 h. The simultaneous administration of cisplatin and GSIs did not reverse the neuronal morphology of SKOV3 CP cells ( A - D ). Additionally, this combination did not lead to significant changes in Notch3 expression ( E ). However, the incubation with both GSIs induced an upregulation of PAX6 and ChgA, with RG-4733 exerting the most pronounced effect. Panel B : combination treatment of MAP4K4i and GSIs in OC Cells. The exposure of OC cells to MAP4K4i did not induce general changes as expected in HES1 protein levels across various OC cell lines. However, both GSIs significantly downregulated HES1 protein expression ( A - D ). Notch3 expression was stimulated by all inhibitors in both SKOV3 WT and SKOV3 CP cells ( E ). In OVCAR-3 and primary OC cells OC236, only the combination of MAP4K4i with RG-4733 synergistically enhanced Notch3 expression ( G - H ). Furthermore, βIII-tubulin expression was strongly stimulated by the MAP4K4i in SKOV3 WT cells, an effect not observed in the resistant SKOV3 CP subline. Nevertheless, the combination of MAP4K4i with GSIs led to an enhanced expression of this neuronal-related structural protein ( I - J ). ChgA expression was slightly repressed in SKOV3 WT cells but enhanced in SKOV3 CP cells after 24 h of MAP4K4 inhibitor treatment. Both GSIs increased ChgA expression, and this effect was slightly potentiated in the presence of the MAP4K4 inhibitor ( K - L ). Abbreviations: M : MAP4K4i; D : DAPT; RG : RG-4733; AU : arbitrary units. Bar graphs represent densitometric analyses of western blots performed to measure protein expression following drug exposure. Results are representative of n = 3 independent experiments.
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    Interfering Notch and <t>MAP4K4</t> signaling pathways in OC cells. Panel A: combination treatment of cisplatin and GSIs. SKOV3 CP cells were treated under the following conditions: ( A ) medium control, ( B ) 2 µg/ml cisplatin, ( C ) 2 µg/ml cisplatin + 5 µM DAPT, and ( D ) 2 µg/ml cisplatin + 1 µM RG-4733 for 120 h. The simultaneous administration of cisplatin and GSIs did not reverse the neuronal morphology of SKOV3 CP cells ( A - D ). Additionally, this combination did not lead to significant changes in Notch3 expression ( E ). However, the incubation with both GSIs induced an upregulation of PAX6 and ChgA, with RG-4733 exerting the most pronounced effect. Panel B : combination treatment of MAP4K4i and GSIs in OC Cells. The exposure of OC cells to MAP4K4i did not induce general changes as expected in HES1 protein levels across various OC cell lines. However, both GSIs significantly downregulated HES1 protein expression ( A - D ). Notch3 expression was stimulated by all inhibitors in both SKOV3 WT and SKOV3 CP cells ( E ). In OVCAR-3 and primary OC cells OC236, only the combination of MAP4K4i with RG-4733 synergistically enhanced Notch3 expression ( G - H ). Furthermore, βIII-tubulin expression was strongly stimulated by the MAP4K4i in SKOV3 WT cells, an effect not observed in the resistant SKOV3 CP subline. Nevertheless, the combination of MAP4K4i with GSIs led to an enhanced expression of this neuronal-related structural protein ( I - J ). ChgA expression was slightly repressed in SKOV3 WT cells but enhanced in SKOV3 CP cells after 24 h of MAP4K4 inhibitor treatment. Both GSIs increased ChgA expression, and this effect was slightly potentiated in the presence of the MAP4K4 inhibitor ( K - L ). Abbreviations: M : MAP4K4i; D : DAPT; RG : RG-4733; AU : arbitrary units. Bar graphs represent densitometric analyses of western blots performed to measure protein expression following drug exposure. Results are representative of n = 3 independent experiments.
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    Interfering Notch and MAP4K4 signaling pathways in OC cells. Panel A: combination treatment of cisplatin and GSIs. SKOV3 CP cells were treated under the following conditions: ( A ) medium control, ( B ) 2 µg/ml cisplatin, ( C ) 2 µg/ml cisplatin + 5 µM DAPT, and ( D ) 2 µg/ml cisplatin + 1 µM RG-4733 for 120 h. The simultaneous administration of cisplatin and GSIs did not reverse the neuronal morphology of SKOV3 CP cells ( A - D ). Additionally, this combination did not lead to significant changes in Notch3 expression ( E ). However, the incubation with both GSIs induced an upregulation of PAX6 and ChgA, with RG-4733 exerting the most pronounced effect. Panel B : combination treatment of MAP4K4i and GSIs in OC Cells. The exposure of OC cells to MAP4K4i did not induce general changes as expected in HES1 protein levels across various OC cell lines. However, both GSIs significantly downregulated HES1 protein expression ( A - D ). Notch3 expression was stimulated by all inhibitors in both SKOV3 WT and SKOV3 CP cells ( E ). In OVCAR-3 and primary OC cells OC236, only the combination of MAP4K4i with RG-4733 synergistically enhanced Notch3 expression ( G - H ). Furthermore, βIII-tubulin expression was strongly stimulated by the MAP4K4i in SKOV3 WT cells, an effect not observed in the resistant SKOV3 CP subline. Nevertheless, the combination of MAP4K4i with GSIs led to an enhanced expression of this neuronal-related structural protein ( I - J ). ChgA expression was slightly repressed in SKOV3 WT cells but enhanced in SKOV3 CP cells after 24 h of MAP4K4 inhibitor treatment. Both GSIs increased ChgA expression, and this effect was slightly potentiated in the presence of the MAP4K4 inhibitor ( K - L ). Abbreviations: M : MAP4K4i; D : DAPT; RG : RG-4733; AU : arbitrary units. Bar graphs represent densitometric analyses of western blots performed to measure protein expression following drug exposure. Results are representative of n = 3 independent experiments.

    Journal: Scientific Reports

    Article Title: The neuroepithelial origin of ovarian carcinomas explained through an epithelial-mesenchymal-ectodermal transition enhanced by cisplatin

    doi: 10.1038/s41598-024-76984-9

    Figure Lengend Snippet: Interfering Notch and MAP4K4 signaling pathways in OC cells. Panel A: combination treatment of cisplatin and GSIs. SKOV3 CP cells were treated under the following conditions: ( A ) medium control, ( B ) 2 µg/ml cisplatin, ( C ) 2 µg/ml cisplatin + 5 µM DAPT, and ( D ) 2 µg/ml cisplatin + 1 µM RG-4733 for 120 h. The simultaneous administration of cisplatin and GSIs did not reverse the neuronal morphology of SKOV3 CP cells ( A - D ). Additionally, this combination did not lead to significant changes in Notch3 expression ( E ). However, the incubation with both GSIs induced an upregulation of PAX6 and ChgA, with RG-4733 exerting the most pronounced effect. Panel B : combination treatment of MAP4K4i and GSIs in OC Cells. The exposure of OC cells to MAP4K4i did not induce general changes as expected in HES1 protein levels across various OC cell lines. However, both GSIs significantly downregulated HES1 protein expression ( A - D ). Notch3 expression was stimulated by all inhibitors in both SKOV3 WT and SKOV3 CP cells ( E ). In OVCAR-3 and primary OC cells OC236, only the combination of MAP4K4i with RG-4733 synergistically enhanced Notch3 expression ( G - H ). Furthermore, βIII-tubulin expression was strongly stimulated by the MAP4K4i in SKOV3 WT cells, an effect not observed in the resistant SKOV3 CP subline. Nevertheless, the combination of MAP4K4i with GSIs led to an enhanced expression of this neuronal-related structural protein ( I - J ). ChgA expression was slightly repressed in SKOV3 WT cells but enhanced in SKOV3 CP cells after 24 h of MAP4K4 inhibitor treatment. Both GSIs increased ChgA expression, and this effect was slightly potentiated in the presence of the MAP4K4 inhibitor ( K - L ). Abbreviations: M : MAP4K4i; D : DAPT; RG : RG-4733; AU : arbitrary units. Bar graphs represent densitometric analyses of western blots performed to measure protein expression following drug exposure. Results are representative of n = 3 independent experiments.

    Article Snippet: In addition, inhibition of MAP4K4 using the small molecule PF-06260933 (MedChemExpress, NJ, USA) enforces the neuroendocrine differentiation of cells in colonic organoids .

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