The endoplasmic reticulum stress transducer old astrocyte specifically induced substance (OASIS) positively regulates glial scar formation in spinal cord injury (SCI). OASIS deletion inhibited the development of N-cadherin-positive reactive astrocytes that form glial scars and promoted axon growth and functional recovery after SCI.
The results suggest that CREB3L1 is required for decidualization in mice and humans and may be linked to the pathogenesis of endometriosis in a progesterone-dependent manner.
OASIS affects the expression of HIF-1alpha target genes through the protein interaction with HIF-1alpha and that OASIS-HIF-1alpha complexes may play essential roles in angiogenesis during bone development.
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