ライフサイエンスコーパス: TGase

1 TGase 1 is a key component of barrier formation in kerat

2 TGase 2 activates NF-kappaB via a novel pathway.

3 TGase 3 isoform is widely expressed and is important for

4 TGase activity is known to be present in the cytosolic,

5 TGase is thought to play a pathogenic role in neurodegen

6 TGase is thought to play a pathogenic role in neurodegen

7 TGase-1, but not TGase-2, -5, and -7, was expressed in R

8 TGase-induced Abeta40 assemblies are resistant to a 1-h

9 TGase-S exhibits no detectable GTP-binding capability, s

10 TGases (enzyme class (EC) 2.3.2.13) normally catalyse th

11 Transglutaminase-1 (TGase-1) is a Ca(2+)-dependent enzyme capable of cross-l

12 s, at least three of which, namely, TGase 1, TGase 2 (tissue transglutaminase), and TGase 3, are pres

13 Transglutaminase 2 (TGase 2) expression is increased in inflammatory disease

14 Epidermal-type Transglutaminase 3 (TGase 3) is a Ca(2+)-dependent enzyme involved in the cr

15 Transglutaminase 3 (TGase 3) is a member of a family of Ca2+-dependent enzym

16 component of the extracellular matrix and a TGase substrate were co-localized on the HPT cell surfac

17 ructural data reveal for the first time in a TGase enzyme that Ca(2+) ions induce structural changes

18 sent study constitutes the first report of a TGase-like enzyme recruited for the assembly of an antib

19 of transglutaminase activity) and TGaseM (a TGase mutant lacking transglutaminase activity).

20 Exposure of cells to a TGase inhibitor or expression of a dominant-negative for

21 n TGase expression, or treating cells with a TGase inhibitor, blocked EGF-stimulated cell migration a

22 nt for EGF to properly localize and activate TGase can be circumvented by the expression of oncogenic

23 ompounds do not inhibit but instead activate TGase 3 transamidation by about 10-fold.

24 e have recently shown that calcium-activated TGase 3, like TGase 2, can bind, hydrolyze, and is inhib

25 MB231, indicating that constitutively active TGase may be a characteristic of certain cancer cells.

26 The crystal structures of active TGase 3 with guanosine 5'-O-(thiotriphosphate) (GTPgamma

27 ptosis is linked to the expression of active TGase.

28 the direct binding of GTP/GDP to the active TGase 3 enzyme, and we show that the TGase 3 enzyme unde

29 Ca(2+)-dependent transglutaminase activity (TGase) that cross-links proteins involved in wound heali

30 cessary for migration and invasive activity, TGase is already at the leading edge and activated.

31 In addition to its transamidation activity, TGase can bind guanosine 5'-triphosphate (GTP) and does

32 g using the AdmF sequence yielded additional TGases in unassigned natural product biosynthetic pathwa

33 We found that EGF stimulation affected TGase expression and activation very differently in thes

34 -2.5 TCR transgenic mice are increased after TGase conversion of the peptide.

35 CEST appeared at -9.2 ppm after TGase conjugated Tm-DO3A-cadaverine to albumin, which al

36 the X-ray crystal structures of TGase-II and TGase-III, we identified three putative Ca(2+)-regulator

37 TGase-1 to induce Stat-3 phosphorylation and TGase-1 potentiates JAK2-induced Stat-3 phosphorylation.

38 se 1, TGase 2 (tissue transglutaminase), and TGase 3, are present in the brain.

39 ssing wild-type, C277S mutant, and antisense TGase), we demonstrate that transglutaminase activity is

40 invasion, while overexpression of antisense TGase blocks RA-induced migration and invasion, indicati

41 here have been a few molecules identified as TGase inhibitors in the past thirty years, none of them

42 reening identified 267 glutamine peptides as TGase-reactive, of which 21 were further analyzed by sol

43 tin and tubulin), while cell wall-associated TGases are believed to regulate pollen tube growth.

44 n a number of cell lines revealed high basal TGase GTP binding activity in tumor cell lines U87 and M

45 Because TGase activity promoted apatite deposition, our findings

46 Because TGase is implicated in protein aggregation, there is evi

47 an interrelationship seems to exist between TGase and PKA-dependent signaling.

48 mically significant forms of substrate-bound TGase exist in equal concentration.

49 ssible signaling pathways may be affected by TGase and result in increased mineralization (i.e., TGF-

50 totic effects of EGF were not compromised by TGase overexpression, and in fact, exogenous TGase expre

51 n; though, when mineralization is induced by TGase, there is no detectible elevation of TGF-beta, sug

52 tion in host cells: protein cross-linking by TGase, tyrosine phosphorylation, PLC-gamma2 activation,

53 e as well as I-kappaBalpha polymerization by TGase 2.

54 g and old chondrocytes and was unaffected by TGase inhibition.

55 encoding a truncated form of TGase-2 (called TGase-S), shows strong apoptotic activity.

56 is truncated at the 3' end, and thus called TGase-short (TGase-S), is cytotoxic.

57 Meniscal cell TGase activity was stimulated by nitric oxide donors and

58 rotein that does not belong to the classical TGase family.

59 l enzyme with transglutaminase crosslinking (TGase), GTP binding, and hydrolysis activities that play

60 ther, these data indicate that a cytoplasmic TGase interacts with the cytoskeleton, while a different

61 In the pollen tube, cytoplasmic TGases are likely to be involved in the incorporation of

62 Binding of cytosolic TGase to actin filaments was shown to be Ca(2+) dependen

63 the expression of the GTP-binding-defective TGase-2 mutants in different cell lines, whereas the exp

64 Moreover, the GTP-binding-defective TGase-2 mutants induced cell death.

65 b(-/-) cells with a transamidation-defective TGase mutant and Rb afforded no protection from HPR-indu

66 d resulted in <10% residual Ca(+2)-dependent TGase activity.

67 The addition of 3 different TGase inhibitors suppressed active TGFbeta1 in the cell

68 cts with the cytoskeleton, while a different TGase isoform, probably delivered via a membrane/cytoske

69 nal electrophoresis indicated that different TGase isoforms were present in distinct subcellular comp

70 t their leading edges, whereas knocking down TGase expression, or treating cells with a TGase inhibit

71 This work supports a role for elevated TGase activity in age-related arthritis based in part on

72 or GTP allowed tTG(V1,2) to exhibit enhanced TGase activity when there is a transient increase in Ca(

73 Exogenous TGase also induces markers of osteoblastic differentiati

74 The exposure of cells expressing exogenous TGase to the PI3K inhibitor, LY294002, reduced the abili

75 TGase overexpression, and in fact, exogenous TGase expression promoted basal cell growth and resistan

76 was determined that expression of exogenous TGase in cells exhibited enhanced GTP binding and transa

77 Moreover, expression of exogenous TGase in SKBR3 cells mimicked the survival advantage of

78 In this study, we show that extracellular TGase activity increased when the ROS level in HPT or AP

79 Finally, TGase-1 was found to interact with JAK2, and this intera

80 creases in detectable CEST effects following TGase-catalyzed conjugation of the contrast agent and pe

81 e development of a mechanism-based assay for TGase and the results of a screen using this assay in wh

82 and determine whether they are essential for TGase-II to confer survival to human breast cancer cells

83 Similar to what we had found for TGase-S, there was a time-dependent decrease in the expr

84 report here a novel pathologic function for TGase in aging articular cartilage.

85 RPTC revealed that JAK2 is indispensable for TGase-1 to induce Stat-3 phosphorylation and TGase-1 pot

86 oup containing the minimal binding motif for TGase 3 that includes a nucleoside recognition groove.

87 ted that the presence of Rb was required for TGase to exhibit anti-apoptotic activity in response to

88 Abeta40 and Abeta42 are good substrates for TGase but show different aggregation patterns.

89 gnaling was necessary but not sufficient for TGase expression.

90 to be useful in identifying other functional TGase inhibitors.

91 However, TGase activity is not antagonistic to EGF signaling.

92 CaM, decreased binding of CaM to mutant htt, TGase-modified htt and cytotoxicity associated with muta

93 Guinea pig and human TGase induced similar Abeta aggregation patterns, and ol

94 GTP-binding capability of full-length human TGase-2 would prevent it from conferring protection agai

95 report the kinetics of interaction of human TGase with one of the inhibitors that we identified, LDN

96 A number of point mutants of human TGase-2 defective for binding GTP, as well as a mutant t

97 Using immunological probes, we identified TGases associated with different subcellular compartment

98 eins mediated by tissue transglutaminase II (TGase), a GTP-binding protein, participating in signal t

99 Tissue transglutaminase II (TGase-II), which is capable of both GTP binding and tran

100 erity-related, and IL-1-induced increases in TGase activity were demonstrated in both knee menisci an

101 Increases in TGase expression and activation often occur in response

102 on velocities of protein-coated particles in TGase-containing water-glycerol solutions were tracked w

103 uggest that the nucleotide binding pocket in TGase 3 may be exploited to either enhance or inhibit th

104 Treatment of HeLa cells with EGF resulted in TGase activation and its accumulation at their leading e

105 nished the ability of EGF and RA to increase TGase protein levels, whereas a constitutively active fo

106 3K) activity was required for RA to increase TGase protein levels.

107 on, and it was recently shown that increased TGase expression protected cells from apoptosis.

108 Indeed, TGase inhibitors prevent depletion of monomeric I-kappaB

109 icate for the first time that EGF can induce TGase expression and activation in human breast cancer c

110 itutively active form of PI3K did not induce TGase expression, indicating that PI3K signaling was nec

111 gate whether EGF also antagonized RA-induced TGase expression in breast cancer cells.

112 ay serve as a survival factor and RA-induced TGase expression requires the activation of PI3K but is

113 n, and it was shown recently that RA-induced TGase expression was inhibited in NIH3T3 mouse fibroblas

114 Not only did EGF fail to block RA-induced TGase expression, but also EGF alone was sufficient to p

115 the actions of EGF and inhibited RA-induced TGase expression, whereas blocking ERK activity in these

116 g these parameters, EGF inhibited RA-induced TGase expression.

117 PI3K activation was necessary for RA-induced TGase expression.

118 Retinoic acid (RA) consistently induces TGase expression and activation, and it was recently sho

119 Retinoic acid (RA) consistently induces TGase expression and activation, and it was shown recent

120 y of each of the TGase inhibitors to inhibit TGase activity.

121 -like molecules for their ability to inhibit TGase.

122 glike compounds for their ability to inhibit TGase.

123 eritoneally entered brain where it inhibited TGase activity.

124 Intriguingly, TGase-S undergoes inappropriate oligomer formation in ce

125 One factor is TGase.

126 We show that although the full-length TGase protein affords strong protection against cell dea

127 y shown that calcium-activated TGase 3, like TGase 2, can bind, hydrolyze, and is inhibited by GTP de

128 d pro-survival signaling pathways to mediate TGase expression and activation.

129 To better understand how RA-mediated TGase expression is regulated, we considered whether co-

130 The membrane TGase is likely associated with both Golgi-derived struc

131 ity that most of the mitochondrial/mitoplast TGase activity is due to TGase 2, the TGase isoform resp

132 The identity of the mitochondrial/mitoplast TGase(s) is not yet known.

133 In an LPS-induced rat brain injury model, TGase inhibitors significantly reduced TNF-alpha synthes

134 ysteines were nitrosylated without modifying TGase activity.

135 me (RhoA inhibitor) or monodansylcadaverine (TGase inhibitor), we show that transamidated RhoA regula

136 nt tissues, at least three of which, namely, TGase 1, TGase 2 (tissue transglutaminase), and TGase 3,

137 Among the nine TGase enzyme isoforms known in the human genome, only TG

138 TGase-1, but not TGase-2, -5, and -7, was expressed in RPTC.

139 inhibitor, LY294002, reduced the ability of TGase to be photoaffinity-labeled with [alpha-(32)P]GTP,

140 ted apoptosis was a result of the ability of TGase to bind GTP and/or catalyze transamidation and fou

141 , these findings suggest that the ability of TGase to modify Rb via transamidation underlies the abil

142 via transamidation underlies the ability of TGase to provide protection against apoptotic insults an

143 substitutions did not affect the ability of TGase-II to bind guanine nucleotides, nor did they cause

144 ion activity is essential for the ability of TGase-II to confer cell survival.

145 same substitutions inhibited the ability of TGase-II to protect human breast cancer cells against th

146 reaction does not compromise the ability of TGase-S to induce cell death.

147 pled with increased expression/activation of TGase and in vivo transamidation and activation of RhoA.

148 f RA signaling, which involves activation of TGase and transamidation of RhoA.

149 The expression and activation of TGase are up-regulated in response to retinoic acid (RA)

150 RA-induced activation of TGase is proposed to induce multiple signaling pathways

151 potent activator of TGASE: The activation of TGase results in increased transamidation of RhoA, which

152 t PI3K regulates the GTP binding activity of TGase as well as its expression.

153 lated expression and GTP binding activity of TGase, thereby linking the up-regulation of TGase with a

154 yed in vitro, the transamidation activity of TGase-II is Ca(2+)-dependent.

155 uggested that the transamidation activity of TGase-II is necessary for the survival of cancer cells c

156 rkedly reduce the GTP hydrolytic activity of TGase-II, mutations at each of the three sites inhibited

157 The apoptotic activity of TGase-S is not dependent on its transamidation activity

158 ltures is stimulated through the addition of TGase, a concomitant reduction (50%) in PKA activity occ

159 Moreover, analysis of TGase expression and GTP binding activity in a number of

160 Association of TGase with the plasma membrane was also confirmed by imm

161 Higher than normal local concentrations of TGase have been correlated with increased protein aggreg

162 14 and significantly lower concentrations of TGase-treated WE14.

163 de evidence that XI is also a consequence of TGase 1 dysfunction.

164 leton integrity, suggesting that delivery of TGase to the cell wall requires the transport of membran

165 gesting a Golgi-based exocytotic delivery of TGase.

166 c inhibitors showed that the distribution of TGase in different subcellular compartments was regulate

167 Biochemical effects of TGase activation, coupled with the formation of stress f

168 XR) agonist (9-cis-RA) promote expression of TGase, migration and invasion of SH-SY5Y cells, while RX

169 ee enzyme, appears to be a common feature of TGase-catalyzed reactions.

170 or expression of a dominant-negative form of TGase potently inhibited EGF-mediated protection from do

171 mer's patients, encoding a truncated form of TGase-2 (called TGase-S), shows strong apoptotic activit

172 t is important for the cellular functions of TGase-II.

173 Immunolocalization of TGase indicated that the enzyme was present in the growi

174 er protein A20) suppressed IL-1 induction of TGase activity.

175 sitide 3-kinase potentiated the induction of TGase expression by EGF in SKBR3 cells.

176 is modification resulted in an inhibition of TGase activity.

177 Inhibition of TGase provides a new treatment strategy for HD and other

178 In the cocultures, inhibition of TGase reduces mineralization, and addition of the enzyme

179 se observations, we found that inhibition of TGase-1 and the JAK2-Stat-3 signaling pathway decreased

180 However, inhibition of TGase-1 decreased phosphorylation of Stat-3 but not JAK2

181 Moreover, inhibition of TGase-modified htt was substrate-specific since overall

182 as a reversible, noncompetitive inhibitor of TGase 3 transamidation activity, similar to GTPgammaS an

183 e demonstrated previously that inhibitors of TGase 2 reduce nitric oxide (NO) generation in a lipopol

184 etreatment of THP-1 cells with inhibitors of TGase, PTK, and PLC.

185 As part of a program to find inhibitors of TGase, we have undertaken kinetic and mechanistic studie

186 We examined the interaction of TGase with the retinoblastoma (Rb) protein, a substrate

187 tate the induction or increase the levels of TGase expression.

188 Thus, at least one mechanism of TGase stimulation probably involves inhibition of the PK

189 The anti-apoptotic mechanisms of TGase are poorly understood at this time.

190 Overexpression of TGase has no effect on migration or invasion, while over

191 Conversely, overexpresssion of TGase-1 enhanced the JAK2-dependent transcriptional acti

192 te glycosylated with GlcN in the presence of TGase at 25 degrees C (FAT25) possessed antioxidant acti

193 TGase, thereby linking the up-regulation of TGase with a well established cell survival factor.

194 ective TGase inhibitor or down-regulation of TGase-1 with small interfering RNA (siRNA) decreased RPT

195 er examine the Ca(2+)-mediated regulation of TGase-II's transamidation activity, with our goals being

196 retreated with RA, an important regulator of TGase.

197 structure determined at 2.0 A resolution of TGase 3 in complex with GMP to elucidate the structural

198 se expression and activation and the role of TGase in these cellular processes are not well understoo

199 In this study, we examined the role of TGase-1 in proliferation of renal proximal tubular cells

200 The potential roles of TGase in this process are investigated and discussed.

201 sons between the X-ray crystal structures of TGase-II and TGase-III, we identified three putative Ca(

202 retinoblastoma (Rb) protein, a substrate of TGase that is also implicated in cell survival functions

203 pounds) of lysine pentapeptide substrates of TGase, synthesized using the "split-mix" method.

204 emonstrating that alternative transcripts of TGase differentially affect cell viability.

205 nst cell death signals, a shorter version of TGase that is truncated at the 3' end, and thus called T

206 s of the effect of amino acid composition on TGase substrates.

207 to stimulate migration is also dependent on TGase.

208 ed three putative Ca(2+)-regulatory sites on TGase-II.

209 yme isoforms known in the human genome, only TGase 2 is known to bind and hydrolyze GTP to GDP; bindi

210 Overexpression of Stat-3, JAK2, and/or TGase-1 in RPTC revealed that JAK2 is indispensable for

211 Treatment with MDC or TGase-1 siRNA decreased Stat-3 but not Akt phosphorylati

212 the activity may be due to one of the other TGase isoforms or perhaps to a protein that does not bel

213 ied htt was substrate-specific since overall TGase activity in the striatum was not altered by treatm

214 alpha in the cytosol of cells overexpressing TGase 2.

215 support of these species being pathological, TGase-induced Abeta40 assemblies (100 nm) inhibited long

216 ions derived from these preparations possess TGase activity.

217 e new assay was conducted to identify potent TGase inhibitors from a 120,000 compound library.

218 s the high-throughput screening of potential TGase inhibitors for antibiotic discovery.

219 that expression of the CaM-fragment reduced TGase-modified htt in the striatum of R6/2 mice.

220 mechanisms used by these stimuli to regulate TGase expression and activation and the role of TGase in

221 was dependent on its ability to up-regulate TGase activity in SKBR3 and BT-20 cells.

222 alone was sufficient to potently up-regulate TGase expression and activation in SKBR3 cells, as well

223 ls restored the ability of RA to up-regulate TGase expression.

224 To better understand how RA regulates TGase, we considered whether RA employed pro-survival si

225 with monodansylcadarevine (MDC), a selective TGase inhibitor or down-regulation of TGase-1 with small

226 at the 3' end, and thus called TGase-short (TGase-S), is cytotoxic.

227 forming growth factor-beta did not stimulate TGase activity.

228 Thus, we studied TGase activity.

229 des an efficient and convenient way to study TGase activities, but also enables the high-throughput s

230 terminal kinase is responsible for targeting TGase to the leading edges of cells and activating it.

231 These findings demonstrate that TGase may serve as a survival factor and RA-induced TGas

232 These findings demonstrate that TGase plays a key role in cancer cell motility and invas

233 These results demonstrate that TGase-1 plays an important role in regulation of renal e

234 We found that TGase 2 activates the transcriptional activator nuclear

235 We report that TGase activity is regulated by NO through a unique Ca(2+

236 In vitro studies revealed that TGase protects Rb from caspase-induced degradation in a

237 Given the role that TGase plays in neurodegenerative disorders, we initiated

238 Here we show that TGase induces rapid aggregation of Abeta within 0.5-30 m

239 Our data suggest that TGase can contribute to AD by initiating Abeta oligomeri

240 ated by environmental stresses, suggest that TGase may function to ensure cell survival under conditi

241 Our data suggest that TGase might constitute a specific therapeutic target for

242 e survival advantage of EGF, suggesting that TGase activation is necessary and sufficient for the ant

243 The TGase 3 isoform is widely expressed and is important for

244 oplast TGase activity is due to TGase 2, the TGase isoform responsible for the majority of the activi

245 for the apoptotic activity exhibited by the TGase-S protein.

246 On the contrary, the TGase cross-linking of milk did not significantly modify

247 further evidence for the pivotal role of the TGase 1 enzyme in CE formation.

248 Administration of the TGase competitive inhibitor, cystamine, to transgenic mi

249 n correlated with the ability of each of the TGase inhibitors to inhibit TGase activity.

250 active TGase 3 enzyme, and we show that the TGase 3 enzyme undergoes a GTPase cycle.

251 s, taken together with observations that the TGase is frequently up-regulated by environmental stress

252 reated cells with LY294002 together with the TGase inhibitor, monodansylcadaverine (MDC), converted R

253 ation and denitrosylation of tTG and thereby TGase activity.

254 at corresponded to peptic fragments of three TGase cross-linked species: Abeta(4-19)--(4-19), Abeta(4

255 utaminases (TGases), Factor XIIIa and tissue TGase (tTGase), are expressed in temporal-spatial associ

256 chondrial/mitoplast TGase activity is due to TGase 2, the TGase isoform responsible for the majority

257 ocal actions of Ca2+ and GTP with respect to TGase 3 activity.

258 Transglutaminase (TGase) catalyzes the calcium-dependent crosslinking of p

259 Transglutaminase (TGase) enzymes catalyze the formation of covalent cross-

260 Transglutaminase (TGase) may be critical in the pathogenesis, via cross-li

261 ere we report that AdmF, a transglutaminase (TGase) homologue, catalyses the formation of the first a

262 e absence or presence of a transglutaminase (TGase) protein cross-linking step on the flavour develop

263 Several active transglutaminase (TGase) isoforms are known to be present in human and rod

264 treatment with the enzyme transglutaminase (TGase).

265 Extracellular transglutaminase (TGase) has been shown previously to play a role in maint

266 in and gene expression for transglutaminase (TGase 2; tissue transglutaminase (tTG)) in hippocampus a

267 d a combinatorial study of transglutaminase (TGase) enzyme substrate peptides, revealing new details

268 the catalytic activity of transglutaminase (TGase), which creates a covalent bond between the agent

269 the presence or absence of transglutaminase (TGase).

270 ing evidence suggests that transglutaminase (TGase) plays a critical role in the pathophysiology of H

271 Tissue transglutaminase (TGase) catalyzes transfer of gamma-acyl moieties of Gln

272 Tissue transglutaminase (TGase) exhibits both a GTP binding/hydrolytic capability

273 potent activator of tissue transglutaminase (TGase) expression, and it was recently shown that phosph

274 Tissue transglutaminase (TGase) has been implicated in neurodegeneration and can

275 Tissue transglutaminase (TGase) is a Ca(2+)-dependent enzyme that catalyzes cross

276 Tissue transglutaminase (TGase) is a Ca2+-dependent enzyme that catalyzes cross-l

277 Tissue transglutaminase (TGase) is a dual function enzyme that couples an ability

278 Tissue transglutaminase (TGase) is involved in the regulation of several biologic

279 However, tissue transglutaminase (TGase) provides an interesting example of a single gene

280 igating the role of tissue transglutaminase (TGase), a protein that has been linked to oncogenesis, i

281 ase) active site of tissue transglutaminase (TGase), eliminated RA protection against cell death and

282 Tissue transglutaminase (TGase-2), which binds GTP and catalyzes the cross-linkin

283 duces expression of tissue-transglutaminase (TGase) and promotes migration and invasion after 24 h of

284 and glucosamine (GlcN) via transglutaminase (TGase), as well as glycation between fish gelatin hydrol

285 had been cross-linked with transglutaminase (TGase) and digested with pepsin.

286 ), monodansylcadaverine (a transglutaminase [TGase] inhibitor), and genistein (a protein tyrosine kin

287 Transglutaminases (TGases) are enzymes that catalyze covalent isopeptide cr

288 Transglutaminases (TGases) are ubiquitous enzymes that take part in a varie

289 Transglutaminases (TGases) are upregulated in hypertrophic chondrocytes, an

290 Two transglutaminases (TGases), Factor XIIIa and tissue TGase (tTGase), are exp

291 Transglycosylase (TGase) is an attractive target for new antibiotic discov

292 operties toward bacterial transglycosylases (TGase).

293 l lines, whereas the expression of wild-type TGase-2 and the GTP hydrolysis-defective mutant was sust

294 To examine whether TGases are involved in regulating mineralization/osteoge

295 However, the precise mechanism by which TGase 2 promotes inflammation remains unclear.

296 tau, alpha-synuclein, and huntingtin) whose TGase-promoted polymerization may be causative in neurod

297 , indicating that other molecules along with TGase mediate RA effects.

298 Western blotting and experiments with TGase 2 knock-out (KO) mice ruled out the possibility th

299 The library was reacted on-resin with TGase enzyme and a soluble desthiobiotin labeled glutami

300 substrates, which was reacted on-resin with TGase enzyme and a soluble desthiobiotin-labeled cadaver