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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Anal+Cell+Pathol+(Amst)
2013 ; 36
(3-4
): 93-105
Nephropedia Template TP
gab.com Text
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English Wikipedia
Cartilage oligomeric matrix protein (COMP)-mediated cell differentiation to
proteolysis mechanism networks from human normal adjacent tissues to lung
adenocarcinoma
#MMPMID24064399
Wang L
; Huang J
; Jiang M
; Diao H
; Zhou H
; Li X
; Chen Q
; Jiang Z
; Feng H
; Wolfl S
Anal Cell Pathol (Amst)
2013[]; 36
(3-4
): 93-105
PMID24064399
show ga
BACKGROUND: To understand cartilage oligomeric matrix protein (COMP) mechanism
network from human normal adjacent tissues to lung adenocarcinoma. METHODS: COMP
complete different activated (all no positive correlation, Pearson CC < 0.25) and
uncomplete (partly no positive correlation except COMP, Pearson CC < 0.25)
network were identified in higher lung adenocarcinoma compared with lower human
normal adjacent tissues from the corresponding COMP-stimulated (?0.25) or
inhibited (Pearson CC ? -0.25) overlapping molecules of Pearson correlation
coefficient (CC) and GRNInfer, respectively. COMP complete different activated
and inhibited (all no positive correlation, Pearson CC < 0.25) mechanisms
networks of higher lung adenocarcinoma and lower human normal adjacent tissues
were constructed by integration of Pearson CC, GRNInfer and GO. As visualized by
integration of GO, KEGG, GenMAPP, BioCarta and Disease, we deduced COMP complete
different activated and inhibited network in higher lung adenocarcinoma and lower
human normal adjacent tissues. RESULTS: As visualized by GO, KEGG, GenMAPP,
BioCarta and disease database integration, we proposed mainly that the mechanism
and function of COMP complete different activated network in higher lung
adenocarcinoma was involved in COMP activation with matrix-localized insulin-like
factor coupling carboxypeptidase to metallopeptidase-induced proteolysis, whereas
the corresponding inhibited network in lower human normal adjacent tissues
participated in COMP inhibition with nucleus-localized vasculogenesis, B and T
cell differentiation and neural endocrine factors coupling
pyrophosphatase-mediated proteolysis. However, COMP complete different inhibited
network in higher lung adenocarcinoma included COMP inhibition with
nucleus-localized chromatin maintenance, licensing and assembly factors coupling
phosphatase-inhibitor to cytokinesis regulators-mediated cell differentiation,
whereas the corresponding activated network in lower human normal adjacent
tissues contained COMP activation with cytolplasm-localized translation
elongation factor coupling fucosyltransferase to ubiquitin-protein ligase-induced
cell differentiation. CONCLUSION: COMP different networks were verified not only
by complete and uncomplete COMP activated or inhibited networks within human
normal adjacent tissues or lung adenocarcinoma, but also by COMP activated and
inhibited network between human normal adjacent tissues and lung adenocarcinoma.