Søren Kragh Moestrup

APOL1 C-Terminal Variants May Trigger Kidney Disease through Interference with APOL3 Control of Actomyosin

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APOL1 C-Terminal Variants May Trigger Kidney Disease through Interference with APOL3 Control of Actomyosin. / Uzureau, Sophie; Lecordier, Laurence; Uzureau, Pierrick; Hennig, Dorle; Graversen, Jonas H.; Homblé, Fabrice; Mfutu, Pepe Ekulu; Oliveira Arcolino, Fanny; Ramos, Ana Raquel; La Rovere, Rita M.; Luyten, Tomas; Vermeersch, Marjorie; Tebabi, Patricia; Dieu, Marc; Cuypers, Bart; Deborggraeve, Stijn; Rabant, Marion; Legendre, Christophe; Moestrup, Søren K.; Levtchenko, Elena; Bultynck, Geert; Erneux, Christophe; Pérez-Morga, David; Pays, Etienne.

In: Cell Reports, Vol. 30, No. 11, 17.03.2020, p. 3821-3836.e13.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Harvard

Uzureau, S, Lecordier, L, Uzureau, P, Hennig, D, Graversen, JH, Homblé, F, Mfutu, PE, Oliveira Arcolino, F, Ramos, AR, La Rovere, RM, Luyten, T, Vermeersch, M, Tebabi, P, Dieu, M, Cuypers, B, Deborggraeve, S, Rabant, M, Legendre, C, Moestrup, SK, Levtchenko, E, Bultynck, G, Erneux, C, Pérez-Morga, D & Pays, E 2020, 'APOL1 C-Terminal Variants May Trigger Kidney Disease through Interference with APOL3 Control of Actomyosin', Cell Reports, vol. 30, no. 11, pp. 3821-3836.e13. https://doi.org/10.1016/j.celrep.2020.02.064

APA

Uzureau, S., Lecordier, L., Uzureau, P., Hennig, D., Graversen, J. H., Homblé, F., Mfutu, P. E., Oliveira Arcolino, F., Ramos, A. R., La Rovere, R. M., Luyten, T., Vermeersch, M., Tebabi, P., Dieu, M., Cuypers, B., Deborggraeve, S., Rabant, M., Legendre, C., Moestrup, S. K., ... Pays, E. (2020). APOL1 C-Terminal Variants May Trigger Kidney Disease through Interference with APOL3 Control of Actomyosin. Cell Reports, 30(11), 3821-3836.e13. https://doi.org/10.1016/j.celrep.2020.02.064

CBE

Uzureau S, Lecordier L, Uzureau P, Hennig D, Graversen JH, Homblé F, Mfutu PE, Oliveira Arcolino F, Ramos AR, La Rovere RM, Luyten T, Vermeersch M, Tebabi P, Dieu M, Cuypers B, Deborggraeve S, Rabant M, Legendre C, Moestrup SK, Levtchenko E, Bultynck G, Erneux C, Pérez-Morga D, Pays E. 2020. APOL1 C-Terminal Variants May Trigger Kidney Disease through Interference with APOL3 Control of Actomyosin. Cell Reports. 30(11):3821-3836.e13. https://doi.org/10.1016/j.celrep.2020.02.064

MLA

Vancouver

Uzureau S, Lecordier L, Uzureau P, Hennig D, Graversen JH, Homblé F et al. APOL1 C-Terminal Variants May Trigger Kidney Disease through Interference with APOL3 Control of Actomyosin. Cell Reports. 2020 Mar 17;30(11):3821-3836.e13. https://doi.org/10.1016/j.celrep.2020.02.064

Author

Uzureau, Sophie ; Lecordier, Laurence ; Uzureau, Pierrick ; Hennig, Dorle ; Graversen, Jonas H. ; Homblé, Fabrice ; Mfutu, Pepe Ekulu ; Oliveira Arcolino, Fanny ; Ramos, Ana Raquel ; La Rovere, Rita M. ; Luyten, Tomas ; Vermeersch, Marjorie ; Tebabi, Patricia ; Dieu, Marc ; Cuypers, Bart ; Deborggraeve, Stijn ; Rabant, Marion ; Legendre, Christophe ; Moestrup, Søren K. ; Levtchenko, Elena ; Bultynck, Geert ; Erneux, Christophe ; Pérez-Morga, David ; Pays, Etienne. / APOL1 C-Terminal Variants May Trigger Kidney Disease through Interference with APOL3 Control of Actomyosin. In: Cell Reports. 2020 ; Vol. 30, No. 11. pp. 3821-3836.e13.

Bibtex

@article{a175f5f60e1b4ed09ce964a70fb05892,
title = "APOL1 C-Terminal Variants May Trigger Kidney Disease through Interference with APOL3 Control of Actomyosin",
abstract = "The C-terminal variants G1 and G2 of apolipoprotein L1 (APOL1) confer human resistance to the sleeping sickness parasite Trypanosoma rhodesiense, but they also increase the risk of kidney disease. APOL1 and APOL3 are death-promoting proteins that are partially associated with the endoplasmic reticulum and Golgi membranes. We report that in podocytes, either APOL1 C-terminal helix truncation (APOL1Δ) or APOL3 deletion (APOL3KO) induces similar actomyosin reorganization linked to the inhibition of phosphatidylinositol-4-phosphate [PI(4)P] synthesis by the Golgi PI(4)-kinase IIIB (PI4KB). Both APOL1 and APOL3 can form K+ channels, but only APOL3 exhibits Ca2+-dependent binding of high affinity to neuronal calcium sensor-1 (NCS-1), promoting NCS-1-PI4KB interaction and stimulating PI4KB activity. Alteration of the APOL1 C-terminal helix triggers APOL1 unfolding and increased binding to APOL3, affecting APOL3-NCS-1 interaction. Since the podocytes of G1 and G2 patients exhibit an APOL1Δ or APOL3KO-like phenotype, APOL1 C-terminal variants may induce kidney disease by preventing APOL3 from activating PI4KB, with consecutive actomyosin reorganization of podocytes.",
keywords = "actomyosin cytoskeleton, APOL1, APOL3, kidney disease, MYH9, NCS-1, phosphoinositide control, PI4KB, sleeping sickness",
author = "Sophie Uzureau and Laurence Lecordier and Pierrick Uzureau and Dorle Hennig and Graversen, {Jonas H.} and Fabrice Hombl{\'e} and Mfutu, {Pepe Ekulu} and {Oliveira Arcolino}, Fanny and Ramos, {Ana Raquel} and {La Rovere}, {Rita M.} and Tomas Luyten and Marjorie Vermeersch and Patricia Tebabi and Marc Dieu and Bart Cuypers and Stijn Deborggraeve and Marion Rabant and Christophe Legendre and Moestrup, {S{\o}ren K.} and Elena Levtchenko and Geert Bultynck and Christophe Erneux and David P{\'e}rez-Morga and Etienne Pays",
year = "2020",
month = mar,
day = "17",
doi = "10.1016/j.celrep.2020.02.064",
language = "English",
volume = "30",
pages = "3821--3836.e13",
journal = "Cell Reports",
issn = "2211-1247",
publisher = "Cell Press",
number = "11",

}

RIS

TY - JOUR

T1 - APOL1 C-Terminal Variants May Trigger Kidney Disease through Interference with APOL3 Control of Actomyosin

AU - Uzureau, Sophie

AU - Lecordier, Laurence

AU - Uzureau, Pierrick

AU - Hennig, Dorle

AU - Graversen, Jonas H.

AU - Homblé, Fabrice

AU - Mfutu, Pepe Ekulu

AU - Oliveira Arcolino, Fanny

AU - Ramos, Ana Raquel

AU - La Rovere, Rita M.

AU - Luyten, Tomas

AU - Vermeersch, Marjorie

AU - Tebabi, Patricia

AU - Dieu, Marc

AU - Cuypers, Bart

AU - Deborggraeve, Stijn

AU - Rabant, Marion

AU - Legendre, Christophe

AU - Moestrup, Søren K.

AU - Levtchenko, Elena

AU - Bultynck, Geert

AU - Erneux, Christophe

AU - Pérez-Morga, David

AU - Pays, Etienne

PY - 2020/3/17

Y1 - 2020/3/17

N2 - The C-terminal variants G1 and G2 of apolipoprotein L1 (APOL1) confer human resistance to the sleeping sickness parasite Trypanosoma rhodesiense, but they also increase the risk of kidney disease. APOL1 and APOL3 are death-promoting proteins that are partially associated with the endoplasmic reticulum and Golgi membranes. We report that in podocytes, either APOL1 C-terminal helix truncation (APOL1Δ) or APOL3 deletion (APOL3KO) induces similar actomyosin reorganization linked to the inhibition of phosphatidylinositol-4-phosphate [PI(4)P] synthesis by the Golgi PI(4)-kinase IIIB (PI4KB). Both APOL1 and APOL3 can form K+ channels, but only APOL3 exhibits Ca2+-dependent binding of high affinity to neuronal calcium sensor-1 (NCS-1), promoting NCS-1-PI4KB interaction and stimulating PI4KB activity. Alteration of the APOL1 C-terminal helix triggers APOL1 unfolding and increased binding to APOL3, affecting APOL3-NCS-1 interaction. Since the podocytes of G1 and G2 patients exhibit an APOL1Δ or APOL3KO-like phenotype, APOL1 C-terminal variants may induce kidney disease by preventing APOL3 from activating PI4KB, with consecutive actomyosin reorganization of podocytes.

AB - The C-terminal variants G1 and G2 of apolipoprotein L1 (APOL1) confer human resistance to the sleeping sickness parasite Trypanosoma rhodesiense, but they also increase the risk of kidney disease. APOL1 and APOL3 are death-promoting proteins that are partially associated with the endoplasmic reticulum and Golgi membranes. We report that in podocytes, either APOL1 C-terminal helix truncation (APOL1Δ) or APOL3 deletion (APOL3KO) induces similar actomyosin reorganization linked to the inhibition of phosphatidylinositol-4-phosphate [PI(4)P] synthesis by the Golgi PI(4)-kinase IIIB (PI4KB). Both APOL1 and APOL3 can form K+ channels, but only APOL3 exhibits Ca2+-dependent binding of high affinity to neuronal calcium sensor-1 (NCS-1), promoting NCS-1-PI4KB interaction and stimulating PI4KB activity. Alteration of the APOL1 C-terminal helix triggers APOL1 unfolding and increased binding to APOL3, affecting APOL3-NCS-1 interaction. Since the podocytes of G1 and G2 patients exhibit an APOL1Δ or APOL3KO-like phenotype, APOL1 C-terminal variants may induce kidney disease by preventing APOL3 from activating PI4KB, with consecutive actomyosin reorganization of podocytes.

KW - actomyosin cytoskeleton

KW - APOL1

KW - APOL3

KW - kidney disease

KW - MYH9

KW - NCS-1

KW - phosphoinositide control

KW - PI4KB

KW - sleeping sickness

UR - http://www.scopus.com/inward/record.url?scp=85081645033&partnerID=8YFLogxK

U2 - 10.1016/j.celrep.2020.02.064

DO - 10.1016/j.celrep.2020.02.064

M3 - Journal article

C2 - 32187552

AN - SCOPUS:85081645033

VL - 30

SP - 3821-3836.e13

JO - Cell Reports

JF - Cell Reports

SN - 2211-1247

IS - 11

ER -