Omi/HtrA2 is a positive regulator of autophagy that facilitates the degradation of mutant proteins involved in neurodegenerative diseases

Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes

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(2009) Congcong He et al.   Annual Review of Genetics

The mitochondrial serine protease HtrA2/Omi: an overview

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The unfolded protein response regulator GRP78/BiP is required for endoplasmic reticulum integrity and stress-induced autophagy in mammalian cells

(2008) J Li et al.   CELL DEATH AND DIFFERENTIATION

Mitochondrial dysfunction triggered by loss of HtrA2 results in the activation of a brain-specific transcriptional stress response

(2008) N Moisoi et al.   CELL DEATH AND DIFFERENTIATION

Omi / HtrA2 is relevant to the selective vulnerability of striatal neurons in Huntington’s disease

(2008) Reina Inagaki et al.   EUROPEAN JOURNAL OF NEUROSCIENCE

Accumulation of HtrA2/Omi in Neuronal and Glial Inclusions in Brains With α-Synucleinopathies

(2008) Yasuhiro Kawamoto et al.   JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY

Hax1-mediated processing of HtrA2 by Parl allows survival of lymphocytes and neurons

(2008) Jyh-Rong Chao et al.   NATURE

Protective role of autophagy in neonatal hypoxia–ischemia induced brain injury

(2008) Silvia Carloni et al.   NEUROBIOLOGY OF DISEASE