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1 plasmic reticulum (ER) stress, we identified salubrinal, a selective inhibitor of cellular complexes
2 A receptor blocker AP-5 or by treatment with salubrinal, a selective inhibitor of eukaryotic translat
7 erference to knock down caspase-12 levels or salubrinal (an ER stress inhibitor) partially protected
8 y, we explored the underlying means by which salubrinal, an activator of eIF2alpha signaling, enhance
9 onnection with ME/CFS, and the potential for salubrinal, an agent known for its influence on cellular
10 ly, treatment of alphaS transgenic mice with Salubrinal, an anti-ER stress compound that delays the o
16 neous or sequential combination therapy with salubrinal, an inhibitor of GADD34-PP1C phosphatase comp
18 induction of the PERK-eIF2alpha pathway with salubrinal attenuated the inflammatory response to both
20 or increasing eIF2alpha phosphorylation with salubrinal did not affect Nrf2 elevation by H(2)O(2).
21 tcome in the surgery-induced ONFH model, and salubrinal improves ONFH symptoms by enhancing angiogene
22 e our understanding of the potential role of salubrinal in improving the quality of life for individu
23 he specific eIF2alpha phosphatase inhibitor, salubrinal, induces resistance against oxidative glutama
27 ion of translational arrest and ER stress by salubrinal or of MAPK signaling pathways attenuate cytok
28 es disposal of reactive oxygen species), and salubrinal (prevents endoplasmic reticulum stress) follo
29 wn inhibitor of eIF2alpha dephosphorylation, salubrinal, revealed that elevated eIF2alpha phosphoryla
30 se 1 a (PP1a)-specific phosphatase inhibitor Salubrinal (SAL) synergized with TG to induce EBV lytic
32 t the ER stress was associated with ONFH and salubrinal significantly improved ONFH-induced symptoms
33 demise by co-treatment with calpastatin and salubrinal suggests co-activation of the calpain and ER-
34 osphorylation with systemically administered salubrinal throughout hypoxia/reoxygenation exposure pre
35 ion of apocynin, tert-butylhydroquinone, and salubrinal to prevent oxidative stress and endoplasmic r
36 rical development and mechanism of action of salubrinal, to mitigate endoplasmic reticulum (ER)/cellu
38 urgery-induced animal model was employed and salubrinal was administered to evaluate the role of ER s
39 avior tests in wild-type mice cotreated with salubrinal (which inhibits translation by inducing eIF2a
40 g eIF2alphaP signaling by the small molecule salubrinal, which inhibits dephosphorylation of eIF2alph