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1 on of a hydrophobic clamp in triosephosphate isomerase.
2 D) is a mitochondrial matrix peptidyl-prolyl isomerase.
3 by serving as an IKK scaffold as well as an isomerase.
4 M17 activity operated by a protein-disulfide isomerase.
5 .5 even in the presence of protein-disulfide isomerase.
6 oxidoreductases ERp57 and protein disulfide isomerase.
7 easome subunits, and isopentenyl diphosphate isomerase.
8 r microcrystals of both naproxen and glucose isomerase.
9 metabolism by inhibition of triose-phosphate isomerase.
10 e ER lumen is prevented by protein disulfide isomerase.
11 s and proteins and is present in other thiol isomerases.
12 ductin1 oxidoreductase and protein disulfide isomerases.
13 the Escherichia coli DsbC and DsbG disulfide isomerases.
14 ep is catalyzed by peptidyl-prolyl cis-trans isomerases.
15 enzymes, such as Delta(3),Delta(2)-enoyl-CoA isomerases.
16 m(7)GTP, and human peptidyl-prolyl cis-trans isomerase 1 (Pin1) in complex with the peptide derived f
17 for an interaction with the peptidyl prolyl isomerase 1 (Pin1), a critical component of PDPK-mediate
18 oring glycolysis (enolase 1, triosephosphate isomerase 1, and hexokinase 2), were reduced when the fu
19 the endomembrane proteins protein disulfide isomerase 5 (PDI5) and NAI2, with the PDI5 interaction b
20 des encoded by the peptidyl-prolyl cis-trans isomerase A (PPIA) gene whose abundance was increased in
21 n A, also known as peptidylprolyl cis-/trans-isomerase A (PPIA), as a foldase is beneficial intracell
22 n A, also known as peptidylprolyl cis-/trans-isomerase A (PPIA), is a mediator of the neuroinflammato
23 serve that the dual-substrate phosphoribosyl isomerase A or priA gene, at which these pathways conver
24 ired Golgi delivery of the protein disulfide isomerase A3 (PDIA3), an enzyme that catalyzes giantin d
27 that in addition to its known histone prolyl isomerase activities, the Fpr4 FKBP domain binds to nucl
30 ing strongly dependent on the peptidylprolyl-isomerase activity and also on the TPR domain of FKBP52,
34 n unfolding, inhibition of PDI reductase and isomerase activity in vitro and in vivo, and subsequent
37 imilarity with Mip proteins, potentiated the isomerase activity of FipB in an in vitro assay and with
39 f FKBP51 requires neither the peptidylprolyl-isomerase activity of the immunophilin nor its associati
42 ant TvCyP1 exhibited typical peptidyl-prolyl isomerase activity with kcat/Km of approximately 7.1 mum
44 to have an additional, unexpected oxidative isomerase activity, thus making it a trifunctional enzym
46 1 reduces the cellular levels of RUNX3 in an isomerase activity-dependent manner by inducing the ubiq
56 des with both CaBP1/P5 and protein disulfide isomerase, although these are generally viewed as compon
57 ion of the BCO-related outlier RPE65 retinol isomerase, an enzyme that does not utilize carotenoids a
58 fied as a secreted peptidyl-prolyl cis/trans isomerase and chaperone that is dispensable for bacteria
59 ER) and is accomplished by protein disulfide isomerase and ER oxidoreductin 1beta, generating stoichi
62 has also been proposed that the ketosteroid isomerase and other enzyme active sites provide electros
66 d RpiB, distant homologs of triose phosphate isomerase and ribose 5-phosphate isomerase B, were neces
67 by this algorithm, genes (ribose 5-phosphate isomerase and ribulose 5-phosphate 3-epimerase) in the p
68 Calvin-Benson cycle enzymes triose-phosphate isomerase and sedoheptulose 1,7-bisphosphate phosphatase
69 ncoded DsbP protein is a bona fide disulfide isomerase and suggest that a dedicated oxidative folding
70 re we show that TaPIN1 is a bona fide prolyl isomerase and that it interacts with the host ubiquitin
71 Next, we expressed a fusion protein of IPP isomerase and the phosphatase (Idi1~NudB) along with a r
74 lysis of the storage, and secretion of thiol isomerases and determination of the electron transfer pa
77 by two proteins with homology to ketosteroid isomerases, and assisted by two proteins with homology t
79 uding a dominant mutation, in RPE65 retinoid isomerase are associated with distinct forms of retinal
82 , ERp5, and ERp57, among perhaps other thiol isomerases, are important for the initiation of thrombus
84 e phosphate isomerase and ribose 5-phosphate isomerase B, were necessary, as previously shown for Rhi
85 rises a major (beta/alpha)8 triose-phosphate isomerase barrel domain and a small alpha + beta inserti
86 novel morbid gene TXNDC15, encoding a thiol isomerase, based on independent loss of function mutatio
87 fringens reveals a modified triose-phosphate isomerase (beta/alpha)8 barrel in which a stable dimer i
88 bridge leading to loss of protein disulfide isomerase binding and lipid transfer activities; however
90 ct types (racemases/epimerases and cis-trans isomerases), but reactions entailing structural isomeris
92 d incomplete equilibrium by triose phosphate isomerase cannot break a (13)C-(13)C bond within the tri
94 lues of (k(cat)/K(m))GAP for triosephosphate isomerase-catalyzed reactions of (R)-glyceraldehyde 3-ph
96 f the flavonoid biosynthetic enzyme chalcone isomerase (CHI), which catalyzes the conversion of narin
97 ibute to the terrestrial plants and chalcone isomerase (CHI)-catalyzed intramolecular and stereospeci
98 reatment with 17l in the glucose-6-phosphate isomerase chronic in vivo mouse model of arthritis yield
99 derstanding of the mechanisms by which thiol isomerases control vascular function, the clinical utili
100 tene isomers in the fruit due to a defective isomerase (CRTISO) and the old gold crimson (og(c) ) tom
103 ontrol) and mice deficient in peptidylprolyl isomerase D (cyclophilin D, encoded by Ppid) by administ
104 ch as Escherichia coli KdsD, contain a sugar isomerase domain and a tandem cystathionine beta-synthas
106 tion was located in the C-terminal disulfide isomerase domain of PDI, sterically close to the enzymat
107 als a central catalytic parvulin-type prolyl isomerase domain, which is inserted into a larger compos
110 onversely, over-expression of the disulphide isomerase DsbA increases the colistin MIC of laboratory
112 nism whereby binding of a substrate to thiol isomerases enhances catalytic activity of remote domains
115 etinyl esters to 11-cis-retinol, is also the isomerase enzyme responsible for the production of meso-
119 thiol isomerases including protein disulfide isomerase, ERp57, and ERp5 are secreted by and localize
122 -regulated protein 78 kDa, protein disulfide isomerase family A, member 6, ER protein 44, and disulfi
123 the oxidation status of ER protein-disulfide isomerase family members revealed a shift to a more oxid
124 ving force for reoxidizing protein disulfide isomerase family members, thus efficiently contributing
128 erium tuberculosis (Mtb) DprE1, an essential isomerase for the biosynthesis of the mycobacterial cell
131 p domains of FipB and FipA impart additional isomerase functionality to FipB, but only the DsbA-like
132 hared mutations: amplification of the xylose isomerase gene and inactivation of ISU1, a gene encoding
133 ry to identify multiple copies of the xylose isomerase gene as a genomic change contributing to high
134 Here we show that the bacterial heptose isomerase GmhA displays homotropic positive and negative
135 d these to show that while protein disulfide isomerase has little capacity for 2dCD4 reduction, Trx r
136 c disulfide bonds that are modified by thiol isomerases have been described in substrates such as alp
137 ines to leucines abolished protein disulfide isomerase heterodimerization, lipid transfer, and apoB s
138 by the cyclophilin family of peptidyl-prolyl isomerases, highlighting the potential for regulation of
145 events replication-dependent removal of Topo-isomerase I-DNA adducts at the step of strand cleavage,
147 desaturase-1, the putative all-trans retinol isomerase in Muller cells, appears to be 9-cis retinol.
150 We have now investigated the role of thiol isomerases in the activation of LLC in platelet releasat
151 There are seven peptidyl-prolyl cis-trans isomerases in the rER, and so far, two of these enzymes,
153 (ii) the DHAP analogue and triose-phosphate isomerase inhibitor phosphoglycolohydroxamate (PGH).
154 adient-2 (AGR2), a soluble protein-disulfide isomerase involved in ER protein folding and quality con
156 tudy, we cloned an isopentenyl pyrophosphate isomerase (IPPI) cDNA, AaIPPI1, from Artemisia annua (Aa
158 e active site base of the enzyme ketosteriod isomerase (KSI) allows efficient and saturable base resc
160 at the active site of the enzyme ketosteroid isomerase (KSI) exerts an extremely large electric field
161 in the active site of the enzyme ketosteroid isomerase (KSI) facilitates quantum proton delocalizatio
162 fluorotyrosines (F-Tyr's) in the ketosteroid isomerase (KSI) oxyanion hole to systematically vary the
165 Depletion of particular ERAD-associated isomerases, lectins, and translocon components, includin
166 we identified variants of PROTEIN DISULFIDE ISOMERASE LIKE 5-1 (HvPDIL5-1) as the cause of naturally
167 or in maize indicated that protein disulfide isomerase-like and phosphoglycerate kinase were required
168 tinct modules: an N-terminal sugar phosphate isomerase-like domain associated with DSD activity and a
169 n the adjacent gene PDILT (protein disulfide isomerase-like, testis expressed) also reached genome-wi
170 sly unappreciated role for Mannose phosphate isomerase (MPI) as a metabolic enzyme required to mainta
171 or CDG-Ib) have mutations in phosphomannose isomerase (MPI) that impair glycosylation and lead to st
172 derived from glucose through phosphomannose isomerase (MPI, Fru-6-P <--> Man-6-P) whose deficiency c
173 ase (MtnP), 5-(methylthio)ribose-1-phosphate isomerase (MtnA), and an annotated class II aldolase-lik
174 with binding of a peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (PIN1) to p53-RS, but not t
175 ng carotenoid isomerase (yofi), a carotenoid-isomerase nonsense mutant, which arrests the turnover of
176 This study provides an overview of which isomerases occur in nature, how we should describe and c
177 pigment epithelium (RPE), is a key retinoid isomerase of the visual cycle necessary for generating 1
179 incomplete equilibration by triose phosphate isomerase, or the transaldolase reaction all interact to
180 ncy of a product analog bound to ketosteroid isomerase oxyanion hole mutants and concluded that the a
182 ave shown that the peptidyl-prolyl cis/trans isomerase parvulin 17 (Par17) interacts with tubulin in
185 his model was dependent on protein disulfide isomerase (PDI) and TF expression by myeloid cells, but
186 gest that the catalysis by protein disulfide isomerase (PDI) and thiol-disulfide exchange is mostly e
188 Thiol isomerases such as protein-disulfide isomerase (PDI) direct disulfide rearrangements required
189 mice generated by crossing protein disulfide isomerase (PDI) floxed mice with lysozyme-Cre transgenic
195 udy was to explain whether protein disulfide isomerase (PDI) is responsible for the thiol-disulfide r
196 e previously reported that protein disulfide isomerase (PDI) is S-nitrosylated in brains of patients
197 ontains >20 members of the protein disulfide isomerase (PDI) superfamily, which ensure formation of t
198 increase in the levels of protein-disulfide isomerase (PDI), a multifaceted endoplasmic reticulum re
199 his enzyme cooperates with protein disulfide isomerase (PDI), a redox chaperone previously implicated
200 ule and lysosome cargo and protein disulfide isomerase (PDI), all of which serve to stabilize thrombu
201 e protein A (NusA), human protein disulphide isomerase (PDI), and the b'a' domain of PDI (PDIb'a').
205 Surprisingly, we find that protein disulfide isomerase (PDI), the major protein oxidase of the ER lum
210 mannosidase Htm1p and the protein disulfide isomerase Pdi1p (Htm1p-Pdi1p) acts as a folding-sensitiv
211 interaction of VWF and the protein disulfide isomerase PDIA1, which has previously been used to visua
217 maintained through action of phosphoglucose isomerase (PGI) and phosphoglucose mutase interconvertin
221 re we identify the peptidyl-prolyl cis-trans isomerase Pin1 as an important factor mediating CPEB des
224 identify a homologue of the peptidyl-prolyl isomerase PIN1 in T. annulata (TaPIN1) that is secreted
225 and a unique therapeutic target, the prolyl isomerase Pin1 is overexpressed in a majority of HCCs, w
226 n was suppressed by inhibitors of the prolyl isomerase Pin1 or extracellular signal-regulated kinases
229 K, conformation of XPO5 is altered by prolyl isomerase Pin1, resulting in reduction of pre-miRNA load
230 regulated by the interaction with the prolyl-isomerase Pin1, via proteasome-mediated degradation; p63
231 ed up-regulation of the expression of prolyl isomerase PIN1, which in turn increases enzyme activity
232 tch3 is a novel target protein of the prolyl-isomerase Pin1, which is able to regulate Notch3 protein
239 osphatase 1B and a peptidyl-prolyl cis-trans isomerase (Pin1) isomerase resulted in potent, selective
241 lpha) is a substrate for the peptidyl prolyl isomerase, Pin1, which mediates cis-trans isomerization
243 cipate in the network pathways linking thiol isomerases, platelet receptor activation, and fibrin gen
244 h as thioredoxin (Trx) and protein disulfide isomerase, play an essential role in regulating the acti
245 not exposed to VCs, plastidic phosphoglucose isomerase (pPGI) acts as an important determinant of pho
247 tilized to confirm peptidyl-prolyl cis-trans-isomerase (PPIase) activity by a PPIase assay and the al
248 Here, we postulated that peptidyl prolyl isomerase (PPIase) activity of FKBP65 positively modulat
249 n A is a conserved peptidyl-prolyl cis-trans isomerase (PPIase) best known as the cellular receptor o
252 RIN4 also interacts with the prolyl-peptidyl isomerase (PPIase) ROC1, which is reduced upon RIN4 Thr1
254 , the rER-resident peptidyl prolyl cis/trans isomerases (PPIases) play an important role in the zippe
257 milies of enzymes, known as "peptidyl-prolyl isomerases" (PPIases), catalyze this reaction, which inv
258 CypA (Cyclophilin A) is a peptidyl-prolyl isomerase previously shown to be required for chondrogen
259 ion, such as calreticulin, protein disulfide isomerase, proteasome subunits, and isopentenyl diphosph
260 racemase), TpiA2 (D-3-tetrulose-4-phosphate isomerase; renamed EryH), and RpiB (D-erythrose-4-phosph
261 med EryH), and RpiB (D-erythrose-4-phosphate isomerase; renamed EryI), a pathway fully consistent wit
262 e report that cyclophilin B (CypB), a prolyl isomerase residing in the endoplasmic reticulum (ER), pr
263 a peptidyl-prolyl cis-trans isomerase (Pin1) isomerase resulted in potent, selective, proteolytically
264 as been proposed to inhibit the visual cycle isomerase RPE65, thereby slowing regeneration of 11-cis-
267 roduce the esterified substrate for retinoid isomerase (RPE65), which converts all-trans-retinyl este
269 comparing the electric field in ketosteroid isomerase's (KSI's) active site to zero overestimates th
270 ters for activation of yeast triosephosphate isomerase (ScTIM), yeast orotidine monophosphate decarbo
273 e more comprehensive identification of thiol isomerase substrates and better elucidation of their cel
278 n-bonding interaction present in ketosteroid isomerase that has been proposed to stabilize a developi
279 D) is a mitochondrial matrix peptidyl-prolyl isomerase that regulates the MPTP and is a drug target f
280 ugh most of the activities of vascular thiol isomerases that contribute to thrombus formation are yet
281 mutant forms to identify substrates of thiol isomerases that participate in the network pathways link
282 our results with those of protein disulfide-isomerase, the eukaryotic counterpart of DsbA, allowing
283 nt four case studies, focused on ketosteroid isomerase, the SH3 domain, dihydrofolate reductase, and
284 he toxin is transferred to protein disulfide isomerase; this ER redox chaperone is known to unfold CT
286 lase 1 family (alpha/beta)8 triose-phosphate isomerase (TIM) barrel structure with a highly conserved
287 end of the HydG (betaalpha)8 triosephosphate isomerase (TIM) barrel, a canonical [4Fe-4S] cluster bin
288 Y208 and S211 from loop 7 of triosephosphate isomerase (TIM) form hydrogen bonds to backbone amides a
291 of the cyclophilin subset of peptidyl-prolyl isomerases to protein folding and identified cyclophilin
292 nophilins, which function as peptidyl-prolyl isomerases, to regulate Crk proteins in human T lymphocy
293 d, namely cystatin B (CSTB), triosephosphate isomerase (TPI1), and deleted in malignant brain tumors
294 17, it was unable to bind protein disulfide isomerase, transfer lipids, and support apoB secretion.
295 In the glycolysis pathway, triosephosphate isomerase was up-regulated, whereas pyruvate kinase was
296 ibitor of the FKBP family of peptidyl prolyl isomerases, was shown to increase survival in animal mod
297 ts with the oxidoreductase protein-disulfide isomerase, we hypothesized that thioredoxin-1 (Trx1), a
298 n-dependent interaction with Pin1, a proline isomerase, which mediates cis-trans isomerization of the
299 ies with double mutants including carotenoid isomerase (yofi), a carotenoid-isomerase nonsense mutant
300 arotene desaturase [ZDS]), and two cis-trans isomerases (zeta-carotene isomerase [ZISO] and prolycope
301 and two cis-trans isomerases (zeta-carotene isomerase [ZISO] and prolycopene isomerase [CrtISO]).
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