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1 tin recognition site within this sequence of tissue transglutaminase.
2 dependent on excess activity of cell surface tissue transglutaminase.
3 l digestion and that have been deamidated by tissue transglutaminase.
4 cells requires deamidation of the protein by tissue transglutaminase.
5 ucts of physiological digestion of gluten by tissue transglutaminase.
6 highly specific substrate for deamidation by tissue transglutaminase.
7 bly occurring as a result of cell leakage of tissue transglutaminase.
8 s to immobilized maltose-binding protein and tissue transglutaminase.
9 ts with a monoclonal antibody raised against tissue transglutaminases.
10 lization of antibodies against epidermal and tissue transglutaminases.
11 830 children tested positive for IgA against tissue transglutaminase (1.0%; 95% confidence interval,
13 tory of celiac disease or antibodies against tissue transglutaminase 2 (controls), healthy family mem
18 isease patients, who have antibodies against tissue transglutaminase 2 in the absence of villous atro
19 st results (for levels of antibodies against tissue transglutaminase-2 and deamidated gliadin peptide
20 , distinct from the two CD hallmark antigens tissue transglutaminase-2 and deamidated gliadin, exhibi
21 s between fibrillar collagens, introduced by tissue transglutaminase-2, are necessary for the self-as
22 le as 60 microU of purified guinea pig liver tissue transglutaminase (4.2 ng or 54 fmol of enzyme).
26 of 60 to 120 kJ per m2 resulted in increased tissue transglutaminase activity when measured either in
29 induced in cortical neurons (ie, cyclin D3, tissue transglutaminase, alpha1-antichymotrypsin, and ST
31 uding serologic tests for antibodies against tissue transglutaminase and deamidated gliadin peptide,
32 strates and/or modulators of enzymes such as tissue transglutaminase and ecto-protein kinases that mo
33 ntion of the profibrotic cleavage substrates tissue transglutaminase and endoglin accompanied MMP-14
35 ed on results of serum tests for IgA against tissue transglutaminase and endomysium or on both a heal
37 The number of cells showing increases in tissue transglutaminase and its cross-link product, epsi
39 In conclusion, IGFBP-1 is a substrate for tissue transglutaminase and Tg leads to the formation of
41 ee or four antibody tests including IgA anti-tissue transglutaminase and/or IgA anti- endomysium perm
42 est results (IgA/IgG gliadin, endomysium, or tissue transglutaminase) and compared them with 213,208
43 st three of which, namely, TGase 1, TGase 2 (tissue transglutaminase), and TGase 3, are present in th
44 ad antibodies against gliadin, 1.22% against tissue transglutaminase, and 0.61% against endomysium (P
45 d peroxidase, gastric parietal cells (PCAs), tissue transglutaminase, and 21-hydroxylase was tested u
46 slinking of VEGF165, catalysed by the enzyme tissue transglutaminase, and associates with MVs through
47 entromere, chromatin, soluble liver antigen, tissue transglutaminase, and deaminated gliadin peptides
48 s (IgA anti-dpgli, IgG anti-dpgli, IgA anti- tissue transglutaminase, and IgA anti-endomysium) yielde
49 though high levels of autoantibodies against tissue transglutaminase (anti-TG2) are strongly indicati
50 d of 10 years and analyzed for antibodies to tissue transglutaminase (anti-TG2A) using a radiobinding
52 iations between levels of antibodies against tissue transglutaminase (anti-tTG, a marker of celiac di
53 (ACPAs), antinuclear antibodies (ANAs), anti-tissue transglutaminase antibodies (AGTAs), and anti-thy
54 oped and optimized for determination of anti-tissue transglutaminase antibodies (anti-tTG) in human s
55 nd specific screening serologic tests (anti- tissue transglutaminase antibodies IgA [anti-TTG] and ed
57 els of soluble E-selectin (sE-sel), IgA anti-tissue transglutaminase antibodies, and serum IL-8 level
58 he sensitivities of Simtomax, endomysial and tissue-transglutaminase antibodies were compared in 133
60 c screening for celiac disease using the IgA tissue transglutaminase antibody (IgA tTG) and, if posit
61 were younger (P = .03), had lower titers of tissue transglutaminase antibody (P = .001), and less fr
62 estigations revealed a slightly elevated IgA tissue transglutaminase antibody level in the setting of
64 t domain revealed that amino acids 81-140 of tissue transglutaminase are involved in fibronectin bind
68 were defined as being positive for islet or tissue transglutaminase autoantibodies at 2 consecutive
69 he TEDDY study who were tested for islet and tissue transglutaminase autoantibodies, respectively.
70 hese results suggest that a risk of islet or tissue transglutaminase autoimmunity need not influence
79 nt upon transglutamination, we determined if tissue transglutaminase could catalyze this reaction and
80 -linking pattern similar to that observed in tissue transglutaminase cross-linked fibrin(ogen) with m
81 ell death with dying cells showing extensive tissue transglutaminase cross-linking of intracellular p
83 nsor based on the covalent immobilization of tissue transglutaminase enzyme in its open conformation
84 roduce cornified envelope precursors and the tissue transglutaminase enzyme that cross-links them.
87 Retinoid and interleukin-6 inductions of tissue transglutaminase expression are mediated by speci
89 r and extracellular compartments elicited by tissue transglutaminase following exposure to ultraviole
90 to Ala significantly reduced the affinity of tissue transglutaminase for fibronectin, indicating that
91 cular mechanisms mediating the regulation of tissue transglutaminase gene expression by TGF-beta fami
92 GF-beta1, BMP2, and BMP4 regulation of mouse tissue transglutaminase gene expression requires a compo
93 t retinoid-dependent expression of the mouse tissue transglutaminase gene is mediated by a versatile
94 oids regulate the transcription of the mouse tissue transglutaminase gene via activation of regulator
98 estinal inflammatory disease, and studies on tissue transglutaminase have generated significant new i
99 en in coeliac disease, and to explore if the tissue transglutaminase homologues found in other organi
101 patients with concentrations of IgA against tissue transglutaminase (IgA-TTG) >10-fold the upper lim
102 ational modification of proteins mediated by tissue transglutaminase II (TGase), a GTP-binding protei
105 ed formation of noncovalent MK multimers nor tissue transglutaminase II covalent multimerization of M
106 the role of the protein cross-linking enzyme tissue transglutaminase in changes associated with the e
108 udy, we have investigated the involvement of tissue transglutaminase in the development of kidney fib
109 eriments clearly demonstrate localization of tissue transglutaminase in the nucleus that can be activ
110 dehydrogenase is less strongly inhibited by tissue transglutaminase in the presence of constructs co
111 3-phosphate dehydrogenase is inactivated by tissue transglutaminase in the presence of glutathione S
112 patients have circulating antibodies against tissue transglutaminase; in children, European guideline
113 disease assay using an assay for IgA against tissue transglutaminase; in subjects with positive test
115 nied by the cross-linking of fibronectin and tissue transglutaminase into nonreducible high molecular
120 stoma SH-SY5Y cells demonstrated that 93% of tissue transglutaminase is localized to the cytosol.
122 rring in rats submitted to SNx suggests that tissue transglutaminase may play an important role in th
124 nt with earlier reports indicating that host tissue transglutaminase modification of gliadin enhances
127 dehydrogenase complex also is inactivated by tissue transglutaminase plus glutathione S-transferase c
129 rs in CV-1 cells demonstrated that the mouse tissue transglutaminase promoter is activated by ligand
131 ly conserved between the human and the mouse tissue transglutaminase promoters and a distal region th
132 s been the discovery of a potential role for tissue transglutaminase, recently found to be the autoan
133 hances gliadin-specific CD T-cell responses, tissue transglutaminase specifically deamidated Q65 in t
134 molecular methodologies to demonstrate that tissue transglutaminase (TG) activates downstream NF-kap
138 g for the inducible enzyme/adhesion molecule tissue transglutaminase (TG), we demonstrate coordinate
139 lcium-dependent protein crosslinking enzyme, tissue transglutaminase (TG2) but no direct link between
145 c expression of the pro-inflammatory protein tissue transglutaminase (TG2) reprograms the transcripti
146 e activity of the matrix crosslinking enzyme tissue transglutaminase (TG2) via S-nitrosylation in you
147 GPR56 inhibits melanoma growth and binds to tissue transglutaminase (TG2), a major crosslinking enzy
150 c breast cancer cells express high levels of tissue transglutaminase (TG2), but established no direct
151 te the performance of antibody tests against tissue transglutaminase (TG2), deamidated gliadin peptid
152 associated with the sulfhydryl-rich protein tissue transglutaminase (TG2), thereby endowing the memb
155 We show that GPR56 binds specifically to tissue transglutaminase, TG2, a widespread component of
156 ptoms and levels of immunoglobulin A against tissue-transglutaminase (TGA-IgA) 10-fold or more the up
159 Retinoic acid (RA) is a potent activator of tissue transglutaminase (TGase) expression, and it was r
166 disease (AD), we investigated the ability of tissue transglutaminase (TGase) to convert human recombi
167 a model system for investigating the role of tissue transglutaminase (TGase), a protein that has been
168 to the enzyme (transamidase) active site of tissue transglutaminase (TGase), eliminated RA protectio
173 lipase Cdelta1 (PLCdelta1) is an effector in tissue transglutaminase (TGII)-mediated alpha1B-adrenore
177 ifferent extents on stiffer substrates; TAZ, tissue transglutaminase (TGM2), and soluble frizzled-rel
178 sensitive fluorometric well plate assay for tissue transglutaminase that is suitable for multiple ki
180 RTX toxin cross-links actin independently of tissue transglutaminase, thus eliminating an indirect mo
181 e as predicted after GC-1g, and the mean IgA-tissue transglutaminase titers declined, contrary to the
183 silon-(gamma-glutamyl) lysine cross-link and tissue transglutaminase took place predominantly in the
186 undergoing short-term antigen challenge and tissue transglutaminase-treated, overlapping synthetic p
187 e dissimilar with known CD-specific antigens tissue transglutaminase (tTG) and deamidated gliadin, an
188 )((app))) of FXIIIa and the guinea pig liver tissue transglutaminase (tTG) and reactivities of Gln su
189 l transglutaminase (TGe) and closely related tissue transglutaminase (tTG) are considered to be autoa
193 d to proteolytic degradation of cell surface tissue transglutaminase (tTG) at the leading edge of mot
194 core protein dimer was determined to be the tissue transglutaminase (tTG) because, first, tTG could
198 (TIMP) expression, stellate cell apoptosis, tissue transglutaminase (tTg) expression, and matrix cro
203 for this defect, we analyzed the activity of tissue transglutaminase (tTG) in TSP-2-null dermal fibro
205 Our previous work showed that cell surface tissue transglutaminase (tTG) induces clustering of inte
212 The recognition scaffold is the following: tissue transglutaminase (tTG) is immobilized as a captur
215 , duodenal biopsy, and serologic analysis of tissue transglutaminase (tTg) levels; endomysial antibod
216 Experimental renal scarring indicates that tissue transglutaminase (tTg) may be associated with the
218 hological crosslinking of alpha-synuclein by tissue transglutaminase (tTG) using immunohistochemistry
219 ometry, glycated haemoglobin (HbA1c) and IgA tissue transglutaminase (tTg) were collected prior to, a
220 ndomysial antibodies (EMA) and antibodies to tissue transglutaminase (tTG) were developed to screen f
221 ne expression for transglutaminase (TGase 2; tissue transglutaminase (tTG)) in hippocampus and isocor
222 n cell lines stably overexpressing wild type tissue transglutaminase (tTG), a mutant inactive tTG, or
223 irected to different antigens, in particular tissue transglutaminase (tTG), gliadin (Glia), and endom
225 ty to bind the protein cross-linking enzyme, tissue transglutaminase (tTG), in cancer cell migration.
227 e repeats are glutaminyl-donor substrates of tissue transglutaminase (tTG), it has been hypothesized
228 sforming growth factor-beta1 (TGF-beta1) and tissue transglutaminase (tTG), two proteins with documen
234 Ca2+-dependent protein cross-linking enzyme tissue transglutaminase (tTGase) is involved in THG-indu
236 they are recognized and deamidated by human tissue transglutaminase (tTGase) with high selectivity.
239 nt increase in liver retinoid concentration, tissue transglutaminase type II (TGaseII) activity, tran
241 2 to more than 12000 participants) found IgA tissue transglutaminase was associated with high accurac
244 These oligomers and those prepared with tissue transglutaminase were used to establish a mechani
245 cellular matrix is stabilized by the enzyme, tissue transglutaminase, which we demonstrated to be ove
246 ification of the fibronectin-binding site on tissue transglutaminase will help to dissect the role of
247 QQDCTLSLQLTT106 inhibited the interaction of tissue transglutaminase with fibronectin and decreased t
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