July 1, 1999Blood

A Requirement for K+-Channel Activity in Growth Factor–Mediated Extracellular Signal-Regulated Kinase Activation in Human Myeloblastic Leukemia ML-1 Cells

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Population

Human myeloblastic leukemia ML-1 cells

Design

Preclinical

Authors

DXDa-Zhong XuSimon Fraser University LWLing WangUniversity of North Carolina at Chapel Hill WDWei DaiRutgers, The State University of New Jersey

Discussion

Member takes

Implication

K+ channel suppression selectively disrupts EGF-driven ERK-2 signaling in animal cells; hypothesis-generating for MAPK-targeted therapies in human cardiovascular disease.

Structured PICO

Population

Human myeloblastic leukemia ML-1 cells

Intervention

Suppression/blockade of K+ channels

Outcome

Activation of extracellular signal-regulated protein kinase 2 (ERK-2) in response to EGF and serumsurrogate

K+ channel activity is required for the initiation of EGF-mediated MAPK pathways, which may explain its association with cell proliferation.

Cite This Study

Xu et al. (1999) studied this question.

synapsesocial.com/papers/6a8a57ffe456f7df1bc1417c https://doi.org/10.1182/blood.v94.1.139.413k11_139_145

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Implication

K+ channel suppression selectively disrupts EGF-driven ERK-2 signaling in animal cells; hypothesis-generating for MAPK-targeted therapies in human cardiovascular disease.

A Requirement for K+-Channel Activity in Growth Factor–Mediated Extracellular Signal-Regulated Kinase Activation in Human Myeloblastic Leukemia ML-1 Cells

Discussion

Member takes

Implication

Structured PICO

Cite This Study

A Requirement for K+-Channel Activity in Growth Factor–Mediated Extracellular Signal-Regulated Kinase Activation in Human Myeloblastic Leukemia ML-1 Cells

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider