hGAAP promotes cell adhesion and migration via the stimulation of store-operated Ca2+ entry and calpain 2

Nuno Saraiva; David L. Prole; Guia Carrara; Benjamin F. Johnson; Colin W. Taylor; Madeline Parsons; Geoffrey L. Smith

doi:10.1083/jcb.201301016

hGAAP promotes cell adhesion and migration via the stimulation of store-operated Ca2+ entry and calpain 2

Nuno Saraiva, David L. Prole, Guia Carrara, Benjamin F. Johnson, Colin W. Taylor, Madeline Parsons, Geoffrey L. Smith^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

43 Citations (Scopus)

Abstract

Golgi antiapoptotic proteins (GAAPs) are highly conserved Golgi membrane proteins that inhibit apoptosis and promote Ca2+ release from intracellular stores. Given the role of Ca2+ in controlling cell adhesion and motility, we hypothesized that human GAAP (hGAAP) might influence these events. In this paper, we present evidence that hGAAP increased cell adhesion, spreading, and migration in a manner that depended on the C-terminal domain of hGAAP. We show that hGAAP increased store-operated Ca2+ entry and thereby the activity of calpain at newly forming protrusions. These hGAAP-dependent effects regulated focal adhesion dynamics and cell migration. Indeed, inhibition or knockdown of calpain 2 abrogated the effects of hGAAP on cell spreading and migration. Our data reveal that hGAAP is a novel regulator of focal adhesion dynamics, cell adhesion, and migration by controlling localized Ca2+-dependent activation of calpain.

Original language	English
Article number	N/A
Pages (from-to)	699-713
Number of pages	15
Journal	Journal of Cell Biology
Volume	202
Issue number	4
DOIs	https://doi.org/10.1083/jcb.201301016
Publication status	Published - 19 Aug 2013

Keywords

BAX INHIBITOR-1
ENDOPLASMIC-RETICULUM
CALCIUM-ENTRY
CALPAIN/CALPASTATIN NETWORK
MEDIATED PROTEOLYSIS
GENE-EXPRESSION
VACCINIA VIRUS
BREAST-CANCER
LIVING CELLS
DYNAMICS

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1083/jcb.201301016

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title = "hGAAP promotes cell adhesion and migration via the stimulation of store-operated Ca2+ entry and calpain 2",

abstract = "Golgi antiapoptotic proteins (GAAPs) are highly conserved Golgi membrane proteins that inhibit apoptosis and promote Ca2+ release from intracellular stores. Given the role of Ca2+ in controlling cell adhesion and motility, we hypothesized that human GAAP (hGAAP) might influence these events. In this paper, we present evidence that hGAAP increased cell adhesion, spreading, and migration in a manner that depended on the C-terminal domain of hGAAP. We show that hGAAP increased store-operated Ca2+ entry and thereby the activity of calpain at newly forming protrusions. These hGAAP-dependent effects regulated focal adhesion dynamics and cell migration. Indeed, inhibition or knockdown of calpain 2 abrogated the effects of hGAAP on cell spreading and migration. Our data reveal that hGAAP is a novel regulator of focal adhesion dynamics, cell adhesion, and migration by controlling localized Ca2+-dependent activation of calpain.",

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author = "Nuno Saraiva and Prole, {David L.} and Guia Carrara and Johnson, {Benjamin F.} and Taylor, {Colin W.} and Madeline Parsons and Smith, {Geoffrey L.}",

year = "2013",

month = aug,

day = "19",

doi = "10.1083/jcb.201301016",

language = "English",

volume = "202",

pages = "699--713",

journal = "Journal of Cell Biology",

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TY - JOUR

T1 - hGAAP promotes cell adhesion and migration via the stimulation of store-operated Ca2+ entry and calpain 2

AU - Saraiva, Nuno

AU - Prole, David L.

AU - Carrara, Guia

AU - Johnson, Benjamin F.

AU - Taylor, Colin W.

AU - Parsons, Madeline

AU - Smith, Geoffrey L.

PY - 2013/8/19

Y1 - 2013/8/19

N2 - Golgi antiapoptotic proteins (GAAPs) are highly conserved Golgi membrane proteins that inhibit apoptosis and promote Ca2+ release from intracellular stores. Given the role of Ca2+ in controlling cell adhesion and motility, we hypothesized that human GAAP (hGAAP) might influence these events. In this paper, we present evidence that hGAAP increased cell adhesion, spreading, and migration in a manner that depended on the C-terminal domain of hGAAP. We show that hGAAP increased store-operated Ca2+ entry and thereby the activity of calpain at newly forming protrusions. These hGAAP-dependent effects regulated focal adhesion dynamics and cell migration. Indeed, inhibition or knockdown of calpain 2 abrogated the effects of hGAAP on cell spreading and migration. Our data reveal that hGAAP is a novel regulator of focal adhesion dynamics, cell adhesion, and migration by controlling localized Ca2+-dependent activation of calpain.

AB - Golgi antiapoptotic proteins (GAAPs) are highly conserved Golgi membrane proteins that inhibit apoptosis and promote Ca2+ release from intracellular stores. Given the role of Ca2+ in controlling cell adhesion and motility, we hypothesized that human GAAP (hGAAP) might influence these events. In this paper, we present evidence that hGAAP increased cell adhesion, spreading, and migration in a manner that depended on the C-terminal domain of hGAAP. We show that hGAAP increased store-operated Ca2+ entry and thereby the activity of calpain at newly forming protrusions. These hGAAP-dependent effects regulated focal adhesion dynamics and cell migration. Indeed, inhibition or knockdown of calpain 2 abrogated the effects of hGAAP on cell spreading and migration. Our data reveal that hGAAP is a novel regulator of focal adhesion dynamics, cell adhesion, and migration by controlling localized Ca2+-dependent activation of calpain.

KW - BAX INHIBITOR-1

KW - ENDOPLASMIC-RETICULUM

KW - CALCIUM-ENTRY

KW - CALPAIN/CALPASTATIN NETWORK

KW - MEDIATED PROTEOLYSIS

KW - GENE-EXPRESSION

KW - VACCINIA VIRUS

KW - BREAST-CANCER

KW - LIVING CELLS

KW - DYNAMICS

U2 - 10.1083/jcb.201301016

DO - 10.1083/jcb.201301016

M3 - Article

C2 - 23940116

SN - 0021-9525

VL - 202

SP - 699

EP - 713

JO - Journal of Cell Biology

JF - Journal of Cell Biology

IS - 4

M1 - N/A

ER -

hGAAP promotes cell adhesion and migration via the stimulation of store-operated Ca2+ entry and calpain 2

Abstract

Keywords

UN SDGs

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