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First-pass extracted concept

HSPA12B

Candidate: concept label1 source documents3 linked claims
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Aliases

Heat shock protein A12B

Evidence Snippets

Heat shock protein A12B (HSPA12B) is mainly expressed in endothelial cells and protects against several harmful factors.
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1knockdown effectsupports2017Source 1DOIPubMed

Knockdown of HSPA12B aggravates lung pathological injury, inflammatory cytokine expression, myeloperoxidase activity, neutrophil infiltration, pulmonary edema, endothelial apoptosis, and worsens survival after CLP surgery.

Quoted textsource-backed
The administration of HSPA12B siRNA aggravated lung pathological injury, upregulated pro-inflammatory cytokine (e.g., IL-1β, TNF-α, and IL-6) expression, and increased myeloperoxidase activity, neutrophil infiltration, pulmonary edema, and pulmonary endothelial cell apoptosis. Additionally, HSPA12B knockdown worsened survival after CLP surgery.
Claim 2mechanistic claimsupports2017Source 1DOIPubMed

The protective mechanism of HSPA12B may partly involve inhibition of ERK phosphorylation and caspase-3 activation in vivo and in vitro.

Quoted textsource-backed
The potential protective mechanisms of HSPA12B may involve the inhibition of ERK phosphorylation and caspase-3 activation in vivo and in vitro.
Claim 3protective rolesupports2017Source 1DOIPubMed

HSPA12B protects vascular endothelial cells against sepsis-induced acute lung injury in mice.

Quoted textsource-backed
HSPA12B protected against sepsis-induced ALI.