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2 rotein, secreted frizzled-related protein 2, Janus kinase 3, and neutral sphingomyelinase 2 proteins
4 tion of STAT3 involves the tyrosine kinases, Janus Kinase-3 as well as Src kinase, whereas the Serine
5 orts, the nonreceptor tyrosine kinase, Jak3 (Janus kinase 3), does not regulate phosphorylation of vi
6 ations are usually absent in the SCID-X1 and Janus kinase 3 forms of SCID and greatly reduced in aden
12 -beta-induced Treg development, and inhibits Janus kinase 3-induced STAT5 phosphorylation, a transcri
13 vide adequate immunosuppression, whereas the Janus kinase 3 inhibitor tofacitinib's success in the tr
15 ing is well known to regulate lymphopoiesis, Janus kinase 3 (JAK3) also plays a critical role in prom
18 tlecitinib, the development of inhibitors of Janus kinase 3 (JAK3) around a putative pyrrolopyrimidin
20 SGs was prevented through the activation of Janus kinase 3 (JAK3) by the vitamin K3 analog menadione
21 yromonas gingivalis enhances the activity of Janus kinase 3 (JAK3) in innate immune cells, and subseq
23 se, p38 kinase, or phosphoinositol 3-kinase, Janus kinase 3 (JAK3) inhibition produced a significant
25 NK cells on SIV infection, use was made of a Janus kinase 3 (JAK3) inhibitor that has previously been
26 sus-host disease (GVHD) prophylaxis with the Janus kinase 3 (JAK3) inhibitor WHI-P131/JANEX-1 on the
33 irement for signaling by multiple cytokines, Janus kinase 3 (JAK3) is an excellent target for clinica
38 microarray-based analyses and showed reduced Janus kinase 3 (JAK3) phosphorylation upon activation.
40 mitogen-activated protein kinase (MAPK), and Janus kinase 3 (JAK3) signaling are necessary for F. tul
42 r of cell lines, and the results showed that Janus kinase 3 (JAK3) was with reduced expression in the
44 ession of a catalytically inactive mutant of Janus kinase 3 (Jak3), and increased in 32D/c-Met cells
45 L7 cells by IL-7 leads to phosphorylation of Janus kinase 3 (JAK3), signal transducer and activator o
46 genesis of colon cancer, nor has the role of Janus kinase 3 (JAK3), the physiological activator of ST
48 lso report that PLD2 is under the control of Janus kinase 3 (JAK3), with the kinase phosphorylating P
49 eficiency (SCID) can be caused by defects in Janus kinase 3 (JAK3)-dependent cytokine signaling pathw
50 nt mutations all resulted in abnormal B-cell Janus kinase 3 (JAK3)-dependent interleukin-2 (IL-2)-ind
51 receptor common gamma chain cytokines and a Janus kinase 3 (JAK3)-dependent pathway in malignant T c
52 ctions during obesity are because of loss of Janus kinase 3 (JAK3)-mediated tyrosine phosphorylation
55 mmac) cytokine-receptor-induced signaling by Janus kinase 3 (Jak3)/stimulators and activators of tran
58 rine systems that in turn activate the Jak3 (Janus kinase 3)/STAT5 (signal transducers and activators