Výsledky vyhledávání - "Jennifer E. Howes"

Supplementary Figure S1 from Small Molecule–Mediated Activation of RAS Elicits Biphasic Modulation of Phospho-ERK Levels that Are Regulated through Negative Feedback on SOS1

Autor: Stephen W. Fesik, Alex G. Waterson, Olivia W. Rossanese, Michael C. Burns, Denis T. Akan, Jennifer E. Howes

Treatment with 1 does not cause total protein levels of SPRY2, SPRY4, DUSP4 and DUSP16 to increase. HeLa cells were treated with 50 μM 1 over a time course of up to 180 minutes. EGF (50 ng/mL for 5 minutes) was used as a positive control. HCT 116 ly

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https://doi.org/10.1158/1535-7163.22505280.v1

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Data from Small Molecule–Mediated Activation of RAS Elicits Biphasic Modulation of Phospho-ERK Levels that Are Regulated through Negative Feedback on SOS1

Autor: Stephen W. Fesik, Alex G. Waterson, Olivia W. Rossanese, Michael C. Burns, Denis T. Akan, Jennifer E. Howes

Oncogenic mutation of RAS results in aberrant cellular signaling and is responsible for more than 30% of all human tumors. Therefore, pharmacologic modulation of RAS has attracted great interest as a therapeutic strategy. Our laboratory has recently

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https://doi.org/10.1158/1535-7163.c.6538014.v1

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Supplementary Figure S3 from Small Molecule–Mediated Activation of RAS Elicits Biphasic Modulation of Phospho-ERK Levels that Are Regulated through Negative Feedback on SOS1

Autor: Stephen W. Fesik, Alex G. Waterson, Olivia W. Rossanese, Michael C. Burns, Denis T. Akan, Jennifer E. Howes

Treatment with 17-AAG does not cause modulation of RAS-GTP levels. HeLa cells were treated with 1 μM 17-AAG over a time course of up to 180 minutes. EGF (50 ng/mL for 5 minutes) was used as a positive control. Two biological repeats of this experime

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https://doi.org/10.1158/1535-7163.22505274

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Supplementary Figure S6 from Small Molecule–Mediated Activation of RAS Elicits Biphasic Modulation of Phospho-ERK Levels that Are Regulated through Negative Feedback on SOS1

Autor: Stephen W. Fesik, Alex G. Waterson, Olivia W. Rossanese, Michael C. Burns, Denis T. Akan, Jennifer E. Howes

SPRY2 is not phosphorylated on tyrosine residues in response to 1 treatment in cells co-expressing V5-SPRY2 and HA-SOS1 S1178A. 293 cells were transiently transfected with both V5-SPRY2 and HA-SOS1 S1178A and treated with 25 μM 1 over a timecourse o

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https://doi.org/10.1158/1535-7163.22505265

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Supplementary Figure S4 from Small Molecule–Mediated Activation of RAS Elicits Biphasic Modulation of Phospho-ERK Levels that Are Regulated through Negative Feedback on SOS1

Autor: Stephen W. Fesik, Alex G. Waterson, Olivia W. Rossanese, Michael C. Burns, Denis T. Akan, Jennifer E. Howes

Modulation of phospho ERK levels is observed at various treatment concentrations of 1. HeLa cells were treated with between 6.25 μM to 100 μM 1 for a time course of up to 30 minutes. Two biological repeats of this experiment were independently cond

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https://doi.org/10.1158/1535-7163.22505271.v1

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Supplementary Figure S5 from Small Molecule–Mediated Activation of RAS Elicits Biphasic Modulation of Phospho-ERK Levels that Are Regulated through Negative Feedback on SOS1

Autor: Stephen W. Fesik, Alex G. Waterson, Olivia W. Rossanese, Michael C. Burns, Denis T. Akan, Jennifer E. Howes

SPRY2 is not phosphorylated on tyrosine residues in response to 1 treatment. 293 cells were transiently transfected with V5-SPRY2 and treated with 25 μM 1 over a timecourse of up to 90 minutes. Where indicated, cells were treated with FBS (20% v/v)

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https://doi.org/10.1158/1535-7163.22505268.v1

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Supplementary Table S1 from Small Molecule–Mediated Activation of RAS Elicits Biphasic Modulation of Phospho-ERK Levels that Are Regulated through Negative Feedback on SOS1

Autor: Stephen W. Fesik, Alex G. Waterson, Olivia W. Rossanese, Michael C. Burns, Denis T. Akan, Jennifer E. Howes

Protein kinase inhibition profile for 1. Compound 1 was tested against a panel of 342 kinases at a single dose concentration of 20 μM. Columns labeled 'Data 1' and 'Data 2' indicate data from technical replicates. Control compound staurosporine was

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https://doi.org/10.1158/1535-7163.22505259

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Supplementary Figure S2 from Small Molecule–Mediated Activation of RAS Elicits Biphasic Modulation of Phospho-ERK Levels that Are Regulated through Negative Feedback on SOS1

Autor: Stephen W. Fesik, Alex G. Waterson, Olivia W. Rossanese, Michael C. Burns, Denis T. Akan, Jennifer E. Howes

Treatment with 1 causes modulation of RAS-GTP and phospho ERK levels in cell lines expressing mutant RAS isoforms. NCI-H1299, NCI-H358, HCT 116 and NCI-H1792 cells were treated with either 25 μM or 50 μM 1 over a time course of up to 180 minutes. E

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https://doi.org/10.1158/1535-7163.22505277

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Small Molecule SOS1 Agonists Modulate MAPK and PI3K Signaling via Independent Cellular Responses

Autor: Edward T. Olejniczak, Jason Phan, Jiqing Sai, Denis T. Akan, Stephen W. Fesik, Alex G. Waterson, Jennifer E. Howes, Allison L. Arnold, Yugandhar Beesetty

Publikováno v: ACS Chemical Biology. 14:325-331

Activating mutations in RAS can lead to oncogenesis by enhancing downstream signaling, such as through the MAPK and PI3K pathways. Therefore, therapeutically targeting RAS may perturb multiple signaling pathways simultaneously. One method for modulat

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0ad555284bbc1811f584a84332f78f6d
https://doi.org/10.1021/acschembio.8b00869

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