member 1 small inducible cytokine subfamily E

Also Known As:

small inducible cytokine subfamily E, member 1; 22-kDa meth A factor; 22-kDa methylcholanthrene A factor; AIMP1 protein, human; EMAP II; EMAP-2; Emap2 protein, mouse; SCYE1 protein, human; Scye1 protein, mouse; Scye1 protein, rat; endothelial monocyte-activating polypeptide II; multisynthetase complex auxiliary component p43; p43 protein, multi-synthetase complex; small inducible cytokine subfamily E, member 1 (endothelial monocyte-activating), human; small inducible cytokine subfamily E, member 1 protein, mouse; small inducible cytokine subfamily E, member 1 protein, rat

Networked: 122 relevant articles (10 outcomes, 28 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	Li, Zhen: 17 articles (01/2018 - 01/2011)
2.	Schwarz, Margaret A: 17 articles (10/2016 - 01/2004)
3.	Wang, Ping: 13 articles (01/2018 - 03/2012)
4.	Schwarz, Roderich E: 11 articles (10/2016 - 07/2004)
5.	Liu, Yunhui: 10 articles (01/2018 - 08/2010)
6.	Xue, Yixue: 10 articles (01/2018 - 08/2010)
7.	Awasthi, Niranjan: 10 articles (10/2016 - 01/2009)
8.	Liu, Libo: 9 articles (01/2018 - 06/2014)
9.	Liu, Yun-hui: 7 articles (02/2016 - 01/2011)
10.	Xue, Yi-xue: 7 articles (02/2016 - 01/2011)

Related Diseases

1.	Neoplasms (Cancer) 04/15/2010 - "In heterotopic PDAC tumors EMAP II caused a significant reduction (>65%) in tumor growth, accompanied by a >50 and 44% decrease in microvessel density and proliferative activity, respectively. " 07/01/2004 - "This feature enables EMAP II to up-regulate the TNF sensitivity of TNF-resistant tumors, an observation of importance in developing new approaches aimed at improving the efficacy of TNF as an anticancer treatment. " 01/01/2017 - "This study was performed to determine whether EMAP II increases the permeability of the blood-tumor barrier (BTB) by affecting the expression of miR-330-3p as well as its possible mechanisms. " 01/01/2018 - "Furthermore, nude mice subjected to miR-24-3p silencing combined with EMAP-II and TMZ treatment displayed the smallest tumors and the longest survival rate. " 06/03/2017 - "Moreover, we found that EMAP-II functioned a targeted suppression on mTOR, which may involve in the anti-neoplasm mechanism. "
2.	Glioblastoma (Glioblastoma Multiforme) 06/03/2017 - "The results suggest that EMAP-II could be considered as a combined chemotherapeutic agent against glioblastoma by sensitizing U87MG and GSCs to TMZ." 01/01/2017 - "Endothelial-Monocyte Activating Polypeptide II Suppresses the In Vitro Glioblastoma-Induced Angiogenesis by Inducing Autophagy." 06/15/2014 - "Anti-neoplastic activity of low-dose endothelial-monocyte activating polypeptide-II results from defective autophagy and G2/M arrest mediated by PI3K/Akt/FoxO1 axis in human glioblastoma stem cells." 01/01/2017 - "Combination of Endothelial-Monocyte-Activating Polypeptide-II with Temozolomide Suppress Malignant Biological Behaviors of Human Glioblastoma Stem Cells via miR-590-3p/MACC1 Inhibiting PI3K/AKT/mTOR Signal Pathway." 11/01/2000 - "Clinical significance of the expression of endothelial-monocyte activating polypeptide II (EMAPII) in the treatment of glioblastoma with recombinant mutant human tumor necrosis factor-alpha (TNF-SAM2)."
3.	Pancreatic Neoplasms (Pancreatic Cancer) 05/01/2010 - "EMAP II-based antiangiogenic-antiendothelial in vivo combination therapy of pancreatic cancer." 04/15/2010 - "Antitumor effects of EMAP II against pancreatic cancer through inhibition of fibronectin-dependent proliferation." 08/01/2009 - "EMAP II had no impact on gemcitabine-induced antiproliferative effects against pancreatic cancer cells in vitro. " 09/01/2011 - "Enhancing cytotoxic agent activity in experimental pancreatic cancer through EMAP II combination therapy." 08/01/2009 - "There was a significant extension of survival after EMAP II and gemcitabine combination therapy compared with controls in 2 different pancreatic cancer cell line models at P = .0001 and P = .006, respectively. "
4.	Sarcoma (Soft Tissue Sarcoma) 09/15/2006 - "In a comparative analysis we found that the overall proEMAP and EMAP-II expression was higher in melanoma as compared to sarcoma cases and measurements in cell lines revealed high proEMAP expression by melanoma cells. " 10/01/2002 - "It has recently been shown that in vivo sensitivity of tumor vasculature to TNF is determined by tumor production of EMAP-II. We measured the level of EMAP-II in a TNF-resistant soft tissue sarcoma. " 10/07/1994 - "A single intra-tumor injection of EMAP II into Meth A sarcomas induced acute thrombohemorrhage and partial tumor regression. " 10/01/2002 - "Improved antitumor response to isolated limb perfusion with tumor necrosis factor after upregulation of endothelial monocyte-activating polypeptide II in soft tissue sarcoma."
5.	Cicatrix (Scar) 02/01/2015 - "We conclude that blockade of EMAP II induces angiogenesis and improves cardiac function following chronic MI, resulting in reduced myocardial fibrosis and scar formation and increased capillary density and preserved viable myocytes in the infarct area." 01/01/2004 - "Six weeks following myocardial infarction, EMAP II protein is elevated above control, changes its location of transcription from the inflammatory cell population to that of the fibroblasts located in the relative avascular scar tissue, and has resumed its perivascular stromal distribution in the viable periinfarct tissue. " 02/01/2015 - "EMAP II AB, compared with vehicle or non-specific antibody, significantly, p<0.05, improved the survival rate after MI, reduced scar size and attenuated the development of heart failure, i.e., left ventricular ejection fraction was significantly higher in EMAP II AB group, fibrosis was reduced by 24%, and importantly, more myocytes were alive in EMAP II AB group in the infarct area. " 01/01/2012 - "Intracellular EMAP II expression is increased during fetal development at epithelial/mesenchymal boundaries and in pathophysiologic fibroproliferative cells of bronchopulmonary dysplasia, emphysema, and scar fibroblast tissue following myocardial ischemia. "

Related Drugs and Biologics

1.	Tumor Necrosis Factor-alpha (Tumor Necrosis Factor)
2.	Gemcitabine
3.	Dexamethasone (Maxidex)
4.	1-phenyl-3,3-dimethyltriazene (PDT)
5.	member 1 small inducible cytokine subfamily E
6.	Peptides (Polypeptides)
7.	rho-Associated Kinases
8.	Cytokines
9.	Proteins (Proteins, Gene)
10.	Biomarkers (Surrogate Marker)

Related Therapies and Procedures

1.	Therapeutics
2.	Topical Administration
3.	Subcutaneous Injections
4.	Percutaneous Coronary Intervention
5.	Glycemic Control