March 31, 2005AJP Cell Physiology

Insulin-activated, K+-channel-sensitive Akt pathway is primary mediator of ML-1 cell proliferation

Q: What is the clinical evidence from this study?

Study design: Other. Population: Myeloblastic leukemia (in vitro). Intervention: 4-aminopyridine (4-AP), barium, and tetraethylammonium. Primary outcome: Cell proliferation and phosphorylation of ERK1/2 and Akt.

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Key result

Suppression of voltage-gated K+ channels with 4-AP inhibited EGF- and insulin-stimulated myeloblastic leukemia ML-1 cell proliferation and prevented phosphorylation of ERK1/2 and Akt.

Population

Myeloblastic leukemia ML-1 cells

Comparison

Voltage-gated K channel suppression with… vs Control

Design

Preclinical

Authors

TGTaylor B. GuoUniversity of California, Los Angeles JLJiawei LuGannan Medical University TLTie LiSouth China Agricultural University

Discussion

Member takes

Implication

K+ channel suppression may curb leukemia cell growth via ERK/Akt; hypothesis-generating, needs in vivo validation before any clinical consideration.

Structured PICO

Population

Myeloblastic leukemia ML-1 cells

Intervention

Voltage-gated K(+) channel suppression with 4-aminopyridine (4-AP), barium, and tetraethylammonium

Comparator

Control (insulin or EGF stimulation without K+ channel blockers)

Outcome

Cell proliferation and phosphorylation of ERK1/2 and Aktsurrogate

Inhibition of voltage-gated K+ channels attenuates insulin-stimulated proliferation of ML-1 leukemia cells by preventing activation of ERK1/2 and Akt pathways.

Cite This Study

Guo et al. (2005) studied Myeloblastic leukemia (in vitro). 4-aminopyridine (4-AP), barium, and tetraethylammonium was evaluated on Cell proliferation and phosphorylation of ERK1/2 and Akt. Suppression of voltage-gated K+ channels with 4-AP inhibited EGF- and insulin-stimulated myeloblastic leukemia ML-1 cell proliferation and prevented phosphorylation of ERK1/2 and Akt.

synapsesocial.com/papers/6aa04987835597572c96889b https://doi.org/10.1152/ajpcell.00010.2005

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March 31, 2005AJP Cell Physiology

Insulin-activated, K+-channel-sensitive Akt pathway is primary mediator of ML-1 cell proliferation

View Full Paper

Ask AI

Bookmark

Key result

Suppression of voltage-gated K+ channels with 4-AP inhibited EGF- and insulin-stimulated myeloblastic leukemia ML-1 cell proliferation and prevented phosphorylation of ERK1/2 and Akt.

Population

Myeloblastic leukemia ML-1 cells

Comparison

Voltage-gated K channel suppression with… vs Control

Design

Preclinical

Authors

TGTaylor B. GuoUniversity of California, Los Angeles JLJiawei LuGannan Medical University TLTie LiSouth China Agricultural University

Discussion

Member takes

Implication

K+ channel suppression may curb leukemia cell growth via ERK/Akt; hypothesis-generating, needs in vivo validation before any clinical consideration.

Structured PICO

Population

Myeloblastic leukemia ML-1 cells

Intervention

Voltage-gated K(+) channel suppression with 4-aminopyridine (4-AP), barium, and tetraethylammonium

Comparator

Control (insulin or EGF stimulation without K+ channel blockers)

Outcome

Cell proliferation and phosphorylation of ERK1/2 and Aktsurrogate

Inhibition of voltage-gated K+ channels attenuates insulin-stimulated proliferation of ML-1 leukemia cells by preventing activation of ERK1/2 and Akt pathways.

Cite This Study

synapsesocial.com/papers/6aa04987835597572c96889b https://doi.org/10.1152/ajpcell.00010.2005

Also Consider

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