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1                                              CNPase and MBP expression was reduced at P15 and remaine
2  nestin and vimentin, and negative for A2B5, CNPase, neurofilament (NF), and neuron specific enolase
3  nestin and vimentin, and negative for A2B5, CNPase, NF, and NSE.
4 rkers neurofilament, GAP-43, synapsin-1, and CNPase--and on the perikarya of sensory neurons in the H
5 chemically GFAP positive, A2B5 negative, and CNPase negative [38].
6 press other oligodendroglial markers such as CNPase, RIP, and APC.
7 re technology was developed to isolate blood CNPase-positive, oligodendrocyte-derived enriched microv
8                                  The central CNPase homology domain was sufficient for catalytic acti
9 s well as the oligodendroglial gene encoding CNPase (2',3' cyclic nucleotide 3'-phosphohydrolase).
10 ostaining for the myelin-synthesizing enzyme CNPase was observed in me/me mice, confirming the loss o
11 neurons, 3) abnormal expression patterns for CNPase and connexin 29 in the SGN clusters, 4) reduced S
12 nuated metabolism of 2',3'-cAMP to 2'-AMP in CNPase(-/-) mice.
13 ial function, number, area, and autophagy in CNPase-knockout (CNPase(-/-)) versus wild-type (WT) mice
14 (IMC-C225) for 2 weeks beginning at birth in CNPase-hEGFR mice normalized all pathologies at 3 months
15  histologic changes were minimal after IR in CNPase(-/-) mice.
16        IR did not affect these parameters in CNPase(-/-) mice.
17 hence the name goldfish regeneration-induced CNPase homolog (gRICH).
18 d accelerated autophagy/mitophagy in injured CNPase(-/-) mice.
19 ber, area, and autophagy in CNPase-knockout (CNPase(-/-)) versus wild-type (WT) mice using a unique t
20 , colocalizing with the Schwann cell marker, CNPase (2',3'-cyclic nucleotide 3'-phosphodiesterase), a
21 , both immature (A2B5+/O4+) and more mature (CNPase+) human oligodendrocytes in vitro expressed the s
22 rentiated into GFAP positive, A2B5 negative, CNPase negative astrocytes, we conclude that 1H91 cells
23 st AKI, it is conceivable that inhibition of CNPase protects against ischemia-reperfusion (IR) -induc
24 lin), astrocyte (GFAP), and oligodendrocyte (CNPase) markers revealed that differentiated neurons con
25 or mature astroglia (GFAP), oligodendroglia (CNPase), or neurons (MAP2).
26 rations in expression of Iba1 or in Olig2 or CNPase.
27 ',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) could be demonstrated for one representative clo
28 ',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) levels, suggesting improved myelin integrity.
29 ',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) metabolizes 2',3'-cAMP to 2'-AMP; 2',3'-cAMP is
30 ',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase; an enzyme that metabolizes 2',3'-cAMP into 2'- a
31 creased cyclic nucleotide phosphodiesterase (CNPase) expression, whereas FGF-2 deprivation alone atte
32 ,3'-cyclic-nucleotide 3'-phosphodiesterases (CNPases), hence the name goldfish regeneration-induced C
33 2;,3;-cyclic nucleotide 3;-phosphohydrolase (CNPase), and vimentin, suggesting that they were not dif
34 ns confirms that both gRICH proteins possess CNPase activity.
35 prolifera-tion in perinatal mutant nerve, so CNPase-hEGFR Schwann cell numbers correlate with the cet
36 y to mammalian myelin marker proteins termed CNPases.
37                             We conclude that CNPase deletion attenuates IR-induced AKI, in part by ac
38 eins are responsible for the majority of the CNPase activity detected in regenerating goldfish retina
39 x17 in the oligodendrocyte lineage under the CNPase promoter.
40                In a mouse model in which the CNPase promoter drives expression of human EGFR in Schwa
41                                        Thus, CNPase enzyme activity is implicated for the first time
42 confirmed with NeuN) or glia (confirmed with CNPase).