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Comment
. 2015 Sep 24;126(13):1519-20.
doi: 10.1182/blood-2015-08-662528.

Neutrophil actin regulation: MKL1 is in control

Affiliations
Comment

Neutrophil actin regulation: MKL1 is in control

Marie-Dominique Filippi. Blood. .

Abstract

In this issue of Blood, Record et al report a novel human primary neutrophil immunodeficiency disorder caused by megakaryoblastic leukemia 1 (MKL1) mutation.

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Conflict of interest statement

Conflict-of-interest disclosure: The author declares no competing financial interests.

Figures

None
Actin dynamics are regulated by numerous stimuli engaging several plasma membrane receptors, including cytokine receptors, G-coupled chemokine receptors, and integrins. Molecules of G-actin sequester MKL1 into the cytoplasm. On stimulation, polymerization of G-actin into F-actin releases MKL1, which can translocate to the cytoplasm and bind nuclear transcription factor SRF. This stimulates expression of cytoskeletal genes, including actin itself and actin regulatory genes. Record et al show that MKL1 notably stimulates the expression of actin, CTTN, formin-binding protein FNBP1L, and myosin light chain (MYL9/MLC). MKL1, together with downstream targets, controls G- and F-actin content, F-actin dynamics, tail retraction, and cell motility.

Comment on

References

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