|1.||Sehgal, Pravin B: 3 articles (10/2013 - 03/2012)|
|2.||Yang, Yang-Ming: 2 articles (02/2013 - 03/2012)|
|3.||Lee, Jason E: 2 articles (02/2013 - 03/2012)|
|4.||Ma, Yong: 1 article (02/2015)|
|5.||Hua, Zhen: 1 article (02/2015)|
|6.||Wang, Jian-Wei: 1 article (02/2015)|
|7.||Yang, Jun-Feng: 1 article (02/2015)|
|8.||Guo, Yang: 1 article (02/2015)|
|9.||Zhang, Ya-Feng: 1 article (02/2015)|
|10.||Gu, Xiao-Lin: 1 article (02/2015)|
|1.||Experimental Autoimmune Encephalomyelitis (Encephalomyelitis, Autoimmune Experimental)
06/01/2009 - "Previous findings demonstrate that neutralization of Nogo, a protein originally identified as a myelin-associated inhibitor (MAI) of axon regeneration, ameliorates experimental autoimmune encephalomyelitis (EAE), a commonly used animal model of MS. More efficient axonal regeneration was suggested as a mechanism underlying the improved EAE outcome. "
|2.||Spinal Cord Injuries (Spinal Cord Injury)
06/01/2007 - "Nogo A protein neutralisation and motor cortex computer implants: a future hope for spinal cord injury."
06/15/2006 - "Therapeutically, targeting the Nogo-A protein by means of the immune response has been tried in an attempt to block neurite growth inhibition and promote regeneration in spinal cord injury models; the immune response to Nogo-A, however, has not been extensively studied. "
02/15/2013 - "Methylprednisolone inhibits Nogo-A protein expression after acute spinal cord injury."
02/01/2015 - "At 24 hours after spinal cord injury, Nogo-A protein and mRNA expression was low in the injured group compared with control and sham-operated groups. "
03/01/2012 - "Acute knockdown of STAT5a/b species using small interfering RNAs (siRNAs), including in the presence of an mRNA synthesis inhibitor (5,6-dichloro-1-β-d-ribofuranosylbenzimidazole), produced a dramatic phenotype within 1 day, consisting of dilatation and fragmentation of Golgi cisternae, a marked tubule-to-cyst change in the ER, increased accumulation of reticulon-4 (RTN4)/Nogo-B and atlastin-3 (ATL3) at cyst-zone boundaries, cystic separation of the outer and inner nuclear membranes, accompanied by scalloped/lunate distortion of the nucleus, with accumulation of RTN4 on convex sides of distorted nuclei. "
10/01/2013 - "Acute siRNA-mediated knockdown of STAT5A/B led to the rapid development of a dramatic cystic change in the endoplasmic reticulum (ER) characterized by deposition of the ER structural protein reticulon-4 (RTN4; also called Nogo-B) and the ER-resident GTPase atlastin-3 (ATL3) along cyst membranes and cyst-zone boundaries, accompanied by Golgi fragmentation. "
02/15/2013 - "In a novel line of research in human pulmonary arterial endothelial cells (HPAECs), we previously observed that STAT5a associated with the Golgi apparatus and that siRNA-mediated knockdown of STAT5a/b led to the rapid development of a dramatic cystic change in the endoplasmic reticulum (ER) characterized by deposition along cyst membranes and tubule-to-cyst boundaries of the proteins reticulon-4 (RTN4; also called Nogo-B) and the ER-resident GTPase atlastin-3 (ATL3) and Golgi fragmentation. "
08/21/2012 - "We investigated the association of Nogo-A protein, a myelin-associated inhibitor of axon regeneration, with secondary damage of the ipsilateral substantia nigra pars reticulata (SNr) after distal middle cerebral artery occlusion (dMCAO) in adult stroke-prone, renovascular hypertensive rats. "
07/01/2008 - "The Nogo-A protein is an important inhibitor of axonal remodeling after central nervous system injuries, including ischemic stroke. "
02/01/2011 - "We also confirmed the overexpression of the Nogo-A protein in 53 astrocytic and oligodendroglial tumors using Western blot analysis. "
06/15/2006 - "In recent years, knowledge about the physiological functions of the Nogo-A protein has grown considerably, and this molecule has evolved from being one of the most important axonal regrowth inhibitors present in central nervous system (CNS) myelin, to several other potentially important roles in different areas such as nervous system development, epilepsy, vascular physiology, muscle pathology and CNS tumors. "
|1.||Messenger RNA (mRNA)
|2.||Small Interfering RNA (siRNA)
|3.||GTP Phosphohydrolases (GTPases)
|4.||Glial Fibrillary Acidic Protein
|5.||Vascular Endothelial Growth Factor A (Vascular Endothelial Growth Factor)
|6.||GAP-43 Protein (GAP 43 Protein)
|7.||Myelin-Associated Glycoprotein (S-MAG)
|8.||Neurotransmitter Receptors (Neurotransmitter Receptor)
|9.||Proteins (Proteins, Gene)