β2-integrins regulate podosome formation as well as nuclear morphology of bone marrow-derived DCs (BMDCs) on both stiff and soft surfaces... loss of β2-integrin adhesion leads to nuclear deformation.
First-pass extracted concept
nuclear deformation
Candidate: concept label1 source documents4 linked claims
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Aliases
nuclear morphology
Evidence Snippets
Supporting Sources
Linked Claims
GADD34 is upregulated in datasets associated with loss of β2-integrin adhesion and nuclear deformation.
Quoted textsource-backed
Growth arrest and DNA damage-inducible protein (GADD34; Ppp1r15) of the unfolded protein responses was also upregulated in both datasets.
Loss of β2-integrin adhesion and nuclear deformation both upregulate dendritic-cell activation markers and cytokines including Ccr7, Cd86, and Il12b.
Quoted textsource-backed
Analysis of published gene expression data revealed that loss of β2-integrin adhesion and nuclear deformation both upregulate DC activation markers and cytokines, including Ccr7, Cd86, and Il12b.
Loss of β2-integrin adhesion leads to nuclear deformation and activation of a cPLA2-GADD34 pathway that partly controls the activated phenotype of bone marrow-derived dendritic cells.
Quoted textsource-backed
Together, our results show that loss of β2-integrin adhesion leads to nuclear deformation and activation of a cPLA2-GADD34 pathway in BMDCs, which at least partly controls their activated phenotype.
β2-integrins regulate podosome formation and nuclear morphology in bone marrow-derived dendritic cells on stiff and soft surfaces.
Quoted textsource-backed
Here, we show that β2-integrins regulate podosome formation as well as nuclear morphology of bone marrow-derived DCs (BMDCs) on both stiff and soft surfaces.