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1 n B sequences were used for cross-linking by TGase 1.
3 The present studies demonstrate that loss of TGase 1 activity is not restricted to mutations that dir
5 the levels of expression and activity of the TGase 1 and 2 enzymes were both increased in the cortex
6 ween SPRs and loricrin, this means that both TGase 1 and 3 are required for cross-linking SPR1 protei
8 atinocyte membranes distort the structure of TGase 1 and facilitate the access of water into its acti
10 se observations, we found that inhibition of TGase-1 and the JAK2-Stat-3 signaling pathway decreased
12 ow here that the equilibrium partitioning of TGase 1 between the cytosol and membranes is controlled
13 We propose a model in which involucrin and TGase 1 bind to membranes shortly after expression in di
15 nto large polymers can occur only by further TGase 1 cross-linking of an initial TGase 3 reaction.
20 we show that the membrane-bound form of the TGase 1 enzyme can also form ester bonds between specifi
28 M1 gene that encodes the transglutaminase 1 (TGase 1) enzyme, which is critical for the assembly of t
29 ation increases the repertoire of functional TGase 1 forms, depending on the differentiation state of
30 Da anchorage fragment facilitates binding of TGase 1 forms, supporting a mechanism of cycling back on
31 homology-derived three-dimensional model of TGase 1 generated from the known x-ray structure of the
40 el system for characterizing the function of TGase 1 on the surface of synthetic lipid vesicles (SLV)
41 However, on SLV carrying both involucrin and TGase 1, only five glutamines serve as donors, of which
44 TGase-1 to induce Stat-3 phosphorylation and TGase-1 potentiates JAK2-induced Stat-3 phosphorylation.
45 -palmitoyl adducts are less than that of the TGase 1 protein, suggesting a mechanism for cycling off
49 nt tissues, at least three of which, namely, TGase 1, TGase 2 (tissue transglutaminase), and TGase 3,
50 c antibodies that in fact three members, the TGase 1, TGase 2, and TGase 3 enzymes, and are different
51 RPTC revealed that JAK2 is indispensable for TGase-1 to induce Stat-3 phosphorylation and TGase-1 pot
53 disease affect the structure and function of TGase 1, we have expressed in baculovirus and keratinocy
54 surface regulates the steric interaction of TGase 1 with substrates such as involucrin to permit spe
55 ective TGase inhibitor or down-regulation of TGase-1 with small interfering RNA (siRNA) decreased RPT
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