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1 of the receptor, STAT1, Janus kinase 1, and tyrosine kinase 2.
2 concomitant phosphorylation of proline-rich tyrosine kinase 2.
3 bitory potency for JAK1 than JAK2, JAK3, and tyrosine kinase 2.
4 activated the downstream kinase proline-rich tyrosine kinase 2.
5 ne phosphatase 1c with the receptor and with tyrosine kinase 2.
6 tein kinase C, Src kinases, and proline-rich tyrosine kinase 2.
7 inhibitor of the BMP6 receptor ALK receptor tyrosine kinase 2/3 or BMP6 siRNA identified BMP6 as a m
8 proteins were identified and include protein-tyrosine kinase 2 (also known as CAKbeta, RAFTK, and CAD
9 e kinase (RAFTK), also known as proline-rich tyrosine kinase 2 and cellular adhesion kinase beta, has
11 associated with diminishing of IL-13-induced tyrosine kinase 2 and signal transducer and activator of
13 mely PKN2 (protein kinase N2), PTK2 (protein tyrosine kinase 2), and ALPP (alkaline phosphatase, plac
15 tyrosine phosphorylation of Janus kinase 2, tyrosine kinase 2, and STAT3 and STAT4 transcription fac
16 contrast, inhibitors of Janus kinase 1/2 and tyrosine kinase 2, as well as the IFN-alpha/beta recepto
18 he phosphorylation and activation of protein-tyrosine kinase 2-beta (PTK2B, also referred to as Pyk2)
19 ing in macrophages, here we identify protein-tyrosine kinase 2-beta (PTK2B/PYK2) as a putative IRF5 k
20 tein 9 (CARD9) disturb the subsequent spleen tyrosine kinase 2-CARD9/BCL10/MALT1-driven signaling cas
22 ntrolene-sensitive, nonreceptor proline-rich tyrosine kinase-2; components of the extracellular signa
25 dicted that the 86 amino acids following the tyrosine kinase 2 domain of beta PDGFR (amino acid resid
26 tyrosine phosphorylation of the proline-rich tyrosine kinase 2, epidermal growth factor receptor (EGF
27 ogen receptor (ER)-positive, erb-b2 receptor tyrosine kinase 2 (ERBB2 [formerly HER2/neu])-negative (
28 , progesterone receptor, and erb-B2 receptor tyrosine kinase 2 (ERBB2 [formerly HER2]) expression, ma
29 AIMS: Drugs that inhibit the erb-b2 receptor tyrosine kinase 2 (ERBB2 or HER2) are the standard treat
31 the cell membrane, and that Erb-b2 receptor tyrosine kinase 2 (Erbb2) function is required for this
32 n, are effective in treating erb-b2 receptor tyrosine kinase 2 (ERBB2)-positive breast cancer (BC) th
33 In a mouse model of basal ErbB2 receptor tyrosine kinase 2 (ErbB2)-positive breast cancer (ErbB2(
36 s regarding the prognosis of erb-b2 receptor tyrosine kinase 2 (ERBB2; formerly HER2 or HER2/neu)-low
37 e receptor (HR)-positive and Erb-B2 receptor tyrosine kinase 2 (ERBB2; formerly HER2 or HER2/neu)-neg
38 mone receptor-negative (HR-)/erb-b2 receptor tyrosine kinase 2 (ERBB2; formerly HER2 or HER2/neu)-pos
39 e receptor (HR)-positive and erb-B2 receptor tyrosine kinase 2 (ERBB2; formerly HER2)-negative breast
40 mRNA expression of discoidin domain receptor tyrosine kinase 2, fibronectin, and alpha-smooth muscle
43 e with a 2538 G-->A missense mutation in the tyrosine kinase-2 gene (Tyk2) are susceptible to Toxopla
44 r protein-tyrosine kinase Pyk2 (proline-rich tyrosine kinase 2) has been shown previously to regulate
45 herapeutic efficacy of human erb-b2 receptor tyrosine kinase 2 (HER2)-specific CAR T cells in an orth
49 ugh its receptor TrkB (neurotrophic receptor tyrosine kinase 2) in the pathophysiology of mood disord
51 2 inhibitors (3.43 [95% CI, 2.14-5.49]), and tyrosine kinase 2 inhibitors (2.64 [95% CI, 1.44-4.86]).
52 The focal adhesion kinase (FAK) gene protein tyrosine kinase 2 is amplified in 16.4% of The Cancer Ge
53 ata further suggest that within this complex tyrosine kinase 2 is the tyrosine kinase responsible for
57 with the BCR-ABL fusion kinase and the Janus tyrosine kinase 2 (JAK2) V617F mutation, respectively.
59 ion of JAKs, all JAKs (JAK1, JAK2, JAK3, and tyrosine kinase 2), JAK2, or JAK3, caused a significant
60 ty, including focal adhesion kinase, protein tyrosine kinase-2, Janus kinase, other focal adhesion-as
64 ion study identified the gene encoding lemur tyrosine kinase-2 (LMTK2) as a susceptibility gene for p
67 in kinase C delta and , but not proline-rich tyrosine kinase 2, mediate tumor necrosis factor alpha-i
69 hat inhibition of both FAK1 and proline-rich tyrosine kinase 2 partially restored integrin beta1 expr
70 r necrosis factor-alpha-induced proline-rich tyrosine kinase 2 phosphorylation, but at different tyro
73 CH patients with higher pretreatment protein tyrosine kinase 2 (PTK2) messenger RNA levels derived gr
74 sion of one such gene, that encoding protein tyrosine kinase 2 (ptk2, also known as focal adhesion ki
75 ion kinase [FAK] family members proline-rich tyrosine kinase 2 [Pyk-2] and FAK) was also examined usi
78 focal adhesion kinase (FAK) and proline-rich tyrosine kinase 2 (Pyk2) and also reduces the associatio
79 nd subsequent activation of the proline rich tyrosine kinase 2 (Pyk2) and Src family kinases, which i
80 focal adhesion kinase (FAK) and proline-rich tyrosine kinase 2 (Pyk2) and their increased association
81 cells, phosphorylation of a FAK/proline-rich tyrosine kinase 2 (PYK2) consensus site in the alpha-hel
82 eceptor tyrosine kinase proline-rich protein tyrosine kinase 2 (Pyk2) functions as an integrator of m
83 tes the role of the nonreceptor proline-rich tyrosine kinase 2 (PYK2) in Ang II-induced VSMC protein
90 in vitro studies indicated that proline-rich tyrosine kinase 2 (PYK2) is a positive mediator of osteo
92 , expression of the FAK-related proline-rich tyrosine kinase 2 (Pyk2) is elevated and phosphorylated
94 study in this issue shows that proline-rich tyrosine kinase 2 (Pyk2) is responsible for acid-induced
97 l that tyrosine kinases Src and proline-rich tyrosine kinase 2 (Pyk2) regulate SHP-1-dependent LPS-in
105 n focal tyrosine kinase (RAFTK)/proline-rich tyrosine kinase 2 (PYK2), an upstream effector of JNK an
106 c TLR9 pathway engagement via MYD88, protein tyrosine kinase 2 (PYK2), and dedicator of cytokinesis 8
107 yrosine-protein kinase) and the proline-rich tyrosine kinase 2 (Pyk2), and they can also cause robust
109 ns of FAK are shared by its homolog, protein tyrosine kinase 2 (Pyk2), raising the question as to whe
110 am focal adhesion kinase (FAK)/ proline-rich tyrosine kinase 2 (PYK2), which are required for myeloid
112 rimary response gene-88 (MYD88)/proline-rich tyrosine kinase 2 (PYK2)/LYN complexes, which allows rec
114 egulated focal adhesion protein proline-rich tyrosine kinase-2 (Pyk2) and the effector proteins paxil
116 hosphorylation (Tyr-402) of the proline-rich tyrosine kinase-2 (PYK2) without significant change in a
117 al adhesion kinase (FAK) and/or proline-rich tyrosine kinase-2 (Pyk2), based on two lines of evidence
118 kinase Cs (aPKCs) by activating proline-rich tyrosine kinase-2 (PYK2), ERK pathway components, and ph
119 inhibitable; (b) dependent upon proline-rich tyrosine kinase-2 (PYK2), GRB2, SOS, RAS, RAF, and MEK1;
120 revious research identified the proline-rich tyrosine kinase 2, Pyk2, as a critical mediator of GC-in
122 dysfunction through inhibition of the IL-13/tyrosine kinase 2/signal transducer and activator of tra
123 al Nrg1 to myocardial ErbB2 (erb-b2 receptor tyrosine kinase 2) signaling and phospho-Erk (phosphoryl
124 cules downstream of the IFN receptor, namely tyrosine kinase 2, STAT1, and IFN regulatory factor 7, a
125 transcription (STAT) family, including JAK1, tyrosine kinase 2, STAT2, and STAT4 in the human progeni
126 that in cells expressing RAFTK/proline-rich tyrosine kinase 2, such as endothelial and B cells, RAFT
127 remodeling pathways (ERBB2 [erbb-b2 receptor tyrosine kinase 2], TGFB1 [transforming growth factor-be
128 ibitory potency for JAK1 than JAK2, JAK3, or tyrosine kinase 2 that is being tested for atopic dermat
129 Y657 of eNOS and expression of proline-rich tyrosine kinase 2 that phosphorylates this residue were
130 G protein and to PLC-gamma via a downstream tyrosine kinase; 2) the initial AT1 receptor-PLC-beta1 c
131 he JAK family includes JAK1, JAK2, JAK3, and tyrosine kinase 2; the STAT family includes STAT1, STAT2
132 NG-2 binds the endothelial-specific receptor tyrosine kinase 2 (TIE2) and acts as a negative regulato
133 ion of the angiopoietin receptor endothelial tyrosine kinase 2 (Tie2) or both angiopoietin-1 and angi
134 -specific tunica intima endothelial receptor tyrosine kinase 2 (Tie2) receptor kinase, angiopoietin-1
136 necrosis factor-alpha activates proline-rich tyrosine kinase 2 to cause cytoskeletal disorganization
138 ly performed genetic screens that identified tyrosine kinase 2 (TYK2) as a candidate regulator of tau
140 ive (CYT387), which inhibits JAK1, JAK2, and tyrosine kinase 2 (TYK2) at low nanomolar concentrations
143 Zasocitinib, a highly selective allosteric tyrosine kinase 2 (TYK2) inhibitor, is a potential new o
149 cule inhibitor with specificity for JAK1 and tyrosine kinase 2 (TYK2) over other JAK family members.
150 mily of cytoplasmic tyrosine kinases) family tyrosine kinase 2 (TYK2) participates in signaling throu
151 cent study, Kim and colleagues decipher that tyrosine kinase 2 (TYK2) phosphorylates tau at tyrosine
153 edictions include a microRNA in an intron of tyrosine kinase 2 (TYK2) that is present in both cat and
155 cure, but we demonstrate that IL-22 acts via tyrosine kinase 2 (Tyk2), a member of the Jak family.
156 components, including Janus kinase 1 (JAK1), tyrosine kinase 2 (Tyk2), and the interferon receptor su
157 tors 1 and 2 (IFNAR1, IFNAR2, respectively), tyrosine kinase 2 (Tyk2), Jak1, and STAT2 are assembled
158 xis, connecting genetic aberrations in FLT3, tyrosine kinase 2 (TYK2), platelet-derived growth factor
159 the pseudokinase domain of the Janus kinase tyrosine kinase 2 (Tyk2), resulting in blockade of recep
160 that MEOX1 knockdown decreased expression of tyrosine kinase 2 (TYK2), signal transducer and activato
164 se family, and brepocitinib, an inhibitor of tyrosine kinase 2 (TYK2)/JAK1 in the treatment of AA.
165 P = 2.3 x 10(-8)) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs21090
166 P = 2.3 x 10(-8)) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3) within
167 Concomitantly, IFN-alpha stimulation of tyrosine kinase 2 tyrosine phosphorylation and kinase ac
169 t al. now show that mutation of another Jak, tyrosine kinase 2, underlies another human immunodeficie
170 comprises four members, JAK1, JAK2, JAK3 and tyrosine kinase 2, which are critical for intracellular
171 small interfering RNA targeting proline-rich tyrosine kinase-2, which was also phosphorylated in resp