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1  fibres, with examples including serpins and cystatins.
2                                Two proteins, cystatin 1 and myeloblastin, the former of which protect
3 le protein with tetratricopeptide repeats 1, cystatin 1, and interferon-inducible protein with tetrat
4 tion is incompatible with previous models of cystatin amyloid fibrils where the beta-sheet is assumed
5  including Tenascins, Cathepsin-B precursor, cystatin, and numerous Variant-specific Surface Proteins
6 ion, and intracellular content of all type 2 cystatins as well as expression and activity of their po
7 and three were successfully verified, namely cystatin B (CSTB), triosephosphate isomerase (TPI1), and
8 y form of cerebral amyloid angiopathy whilst cystatin B aggregates are found in cases of Unverricht-L
9         Here we apply limited proteolysis to cystatin B amyloid fibrils and show that not only the al
10                             Previous work on cystatin B amyloid fibrils revealed that the alpha-helic
11                                              Cystatin B deletion in TgCRND8 significantly reduces the
12         We show that decreased expression of cystatin B in patient fibroblasts enhances cathepsin act
13 of lipid accumulation in TgCRND8 by removing cystatin B inhibition on lysosomal proteases suggests th
14 with available data for amyloids from either cystatin B or cystatin C.
15 m ROS was attenuated in an NPC cell model by cystatin B over-expression or pharmacological inhibition
16                                              Cystatin B was recently identified as an acid-resistant
17                                    Stefin B (cystatin B) is an endogenous cysteine cathepsin inhibito
18 ied the effects of diminishing expression of cystatin B, an endogenous inhibitor of cathepsins B, H a
19 eletion of the lysosomal protease inhibitor, cystatin B.
20 ed to the cytosol, where the CTSB inhibitors cystatin-B/C were abundantly present.
21 at least partially parallel, arrangement for cystatin beta-sheet structure in mature amyloids and pro
22 y C-reactive protein greater than 3.0 mg/dL, cystatin C >/=1.11 mg/dL, estimated glomerular filtratio
23 tin vs placebo; P = .033) and decreased mean cystatin C (-0.034 mg/L vs 0.010 mg/L; P = .008).
24 rs911119 was associated with decreased serum cystatin C (6.13% per allele; 95% CI: 5.75 to 6.50; p =
25 l relative risk for CVD of 1.00 per doubling cystatin C (95% CI: 0.82 to 1.22; p = 0.994), which was
26 alysis, we examined the relationship between cystatin C (a marker of renal function) and PASP and pot
27 igher than SCr (AUC-ROC=0.73) and similar to cystatin C (AUC-ROC=0.91).
28                      We investigated whether cystatin C (CysC) and neutrophil gelatinase-associated l
29 tion rate (GFR) equations incorporating both cystatin C (CysC) and serum creatinine (Creat) in living
30                                              Cystatin C (CysC) is a better glomerular filtration rate
31                                              Cystatin C (CysC) is a versatile and ubiquitously-expres
32 t renal function measures are imperfect, and cystatin C (CysC) is promoted as a better marker of glom
33 ating fragments but is potently inhibited by cystatin C (CysC).
34 tB is inhibited by its endogenous inhibitor, cystatin C (CysC).
35 ed GFR estimated from creatinine (eGFR(Cr)), cystatin C (eGFR(Cys)), or both (eGFR(Cr+Cys)) with ioth
36 e Epidemiology Collaboration eGFR creatinine-cystatin C (eGFRcreat-cys) equation.
37                                      eGFR by cystatin C (eGFRcys) and albumin-to-creatinine ratio wer
38  GFR should be calculated and reported using cystatin C (eGFRcys) and serum creatinine (eGFRcr-cys) o
39 d GFR estimated from creatinine (eGFRcreat), cystatin C (eGFRcys), and both (eGFRcreat-cys) at baseli
40 dominant disorder in which a variant form of cystatin C (L68Q) readily forms amyloid deposits in cere
41 imilarly, both in patients with high and low cystatin C (median cut-off), higher plasma NGAL levels w
42 le risk prediction model, eGFR (P=0.616) and cystatin C (P=0.937) were no longer associated with mort
43 8.30-21.2); Pnoninferiority = 0.0011], serum cystatin C (Pnoninferiority < 0.0001), serum creatinine
44 n decline of eGFR (Ptrend<0.001) and rise of cystatin C (Ptrend=0.01) and creatinine (Ptrend<0.001) l
45 ive protein -0.0363 (95% CI 0.0601--0.0124), cystatin C -0.0391 (95% CI -0.0772--0.00107).
46 bining a functional damage biomarker (plasma cystatin C [pCysC]) with a tubular damage biomarker (uri
47                       All cells internalized cystatin C added to culture media, leading to increased
48 , we developed estimating equations based on cystatin C alone and in combination with creatinine in d
49                                   The use of cystatin C alone or in combination with creatinine stren
50 lculated by the measurement of creatinine or cystatin C alone or in combination with creatinine, with
51 e offspring, suggesting the presence of L68Q cystatin C amyloid affected sperm function.
52                                   Hereditary cystatin C amyloid angiopathy is an autosomal dominant d
53               L68Q protein deposits in human cystatin C amyloid angiopathy patients have also been fo
54                                In hereditary cystatin C amyloid angiopathy, a cystatin C variant is d
55 d causes a fatal amyloid disease, hereditary cystatin C amyloid angiopathy.
56 howed increased levels and distinct forms of cystatin C amyloid that were not present in WT mice.
57                                              Cystatin C amyloids cause a hereditary form of cerebral
58   L68Q epididymal fluid that was depleted of cystatin C amyloids, however, did not impair the motilit
59 cohorts (n = 76,481) with 37,126 measures of cystatin C and added genetic data from 43 studies (n = 2
60                                       Higher cystatin C and beta trace protein associated with a high
61 m underlying the strong relationship between cystatin C and cardiovascular risk.
62 ult ICU survivors, we compared ICU discharge cystatin C and creatinine and their association with 1-y
63                  During ICU admission, serum cystatin C and creatinine diverged, so that by ICU disch
64 d to determine the association between serum cystatin C and mortality.
65 espectively, of the indirect effects between cystatin C and PASP.
66      Rosuvastatin 10 mg daily reduces plasma cystatin C and slows kidney function decline in HIV-infe
67 highly ordered, domain-swapped assemblies of cystatin C and that the oligomers could not build larger
68    Here we aimed to investigate if uptake of cystatin C and the related inhibitor cystatin E/M occur
69     Conversely, lower creatinine relative to cystatin C appeared to confer adverse prognosis, confoun
70 herapeutics targeted at lowering circulating cystatin C are unlikely to be effective in preventing CV
71 implications for the diagnostic use of serum cystatin C as a marker of kidney function during inflamm
72 isual readout and applied it to an assay for cystatin C as a model target.
73            Whilst there is good evidence for cystatin C being a marker of GFR and risk in people with
74 red childhood kidney volumes, creatinine and cystatin C blood levels, microalbuminuria, BP, and eGFR.
75                          Statins may improve cystatin C by improving glomerular function or by decrea
76 m2, calculated using the combined creatinine-cystatin C CKD-Epidemiology Collaboration Equation.
77 ss than 60 mL/min/1.73 m when estimated from cystatin C compared with glomerular filtration rate esti
78 baseline and 0- to 24-week changes in plasma cystatin C concentration with measures of vascular disea
79                                              Cystatin C concentrations remained normal in both groups
80                                              Cystatin C concentrations were associated with CVD risk
81 ation rate (eGFR) using serum creatinine and cystatin C concentrations, and microalbuminuria using ur
82                   In contrast to creatinine, cystatin C consistently associated with long-term mortal
83          Within the statin group, changes in cystatin C correlated with changes in endothelial activa
84 e intracellular concentration of ROS inhibit cystatin C dimerization.
85    These could be used to selectively remove cystatin C dimers from biological fluids containing both
86 diagnostic performance of CKD-EPI creatinine-cystatin C equation (2012) in patients with cirrhosis wa
87    Performance of the new CKD-EPI creatinine-cystatin C equation (2012) was superior to previous crea
88               Accuracy of CKD-EPI creatinine-cystatin C equation as quantified by root mean squared e
89 ubjects, GFR estimated by CKD-EPI creatinine-cystatin C equation differed from the mGFR by more than
90 te the performance of the CKD-EPI creatinine-cystatin C equation in subjects with cirrhosis, we compa
91                      The combined creatinine-cystatin C equation performed better than equations base
92 and "accuracy" of the new CKD-EPI creatinine-cystatin C equation to that of 24-hour urinary creatinin
93                                              Cystatin C forms non-inhibitory dimers and aggregates by
94 ongestion end point) and the change in serum cystatin C from enrollment to 72 hours (renal function e
95              Furthermore, immunodepletion of cystatin C from the conditioned medium completely remove
96                                        Serum cystatin C has an important role in enhancing accuracy o
97  from serum concentrations of creatinine and cystatin C has been refined using cross-sectional data f
98 ne the extent to which the addition of serum cystatin C improves glomerular filtration rate (GFR) est
99 vation and inflammation were associated with cystatin C in a multivariable model independent of creat
100 l variable to investigate the causal role of cystatin C in CVD, including coronary heart disease, isc
101  (from 0.64 (49 nM) to 0.96 mg/L (74 nM)) of cystatin C in serum.
102 on analyses did not support a causal role of cystatin C in the etiology of CVD.
103  cell types synthesize monomeric and dimeric cystatin C in vivo, but only secrete monomer.
104 ile serum creatinine fell at 12 hours, serum cystatin C increased, suggestive of decreased creatinine
105  prostate cancer cells corroborated that the cystatin C internalization is generally relevant and con
106 iological studies show that high circulating cystatin C is associated with risk of cardiovascular dis
107 ndelian randomization to investigate whether cystatin C is causally related to CVD in the general pop
108              The cysteine protease inhibitor cystatin C is internalized by some cancer cells, which a
109                            Low extracellular cystatin C is linked to pathologic protease activity in
110                                           If cystatin C is not available, the BIS1 equation is an acc
111              The cysteine protease inhibitor cystatin C is thought to be secreted by most cells and e
112 he extracellular concentration of inhibitory cystatin C is thus partly dependent on the abundance of
113 714 to 1171 mL; P = .59) or on the change in cystatin C level (dopamine, 0.12 mg/L; 95% CI, 0.06-0.18
114 618 to 1176 mL; P = .49) or on the change in cystatin C level (nesiritide, 0.07 mg/L; 95% CI, 0.01-0.
115 ely associated with childhood creatinine and cystatin C levels (all P values <0.05), but did not asso
116 re media, leading to increased intracellular cystatin C levels by 120-200%.
117 ells are major contributors to extracellular cystatin C levels in healthy mice.
118 filtration rate (GFR) was estimated based on cystatin C levels using the relevant equation.
119 ated on the basis of creatinine (eGFRcr) and cystatin C levels were assessed in </=1735 participants
120                                              Cystatin C levels were positively and plasma high-densit
121     After adjustment for both creatinine and cystatin C levels, higher discharge creatinine was then
122 easured GFR from standardized creatinine and cystatin C levels, sex, and age in the learning sample;
123 ut cirrhosis using both serum creatinine and cystatin C levels.
124 munodeficiency virus (HIV) infection, plasma cystatin C may be influenced by factors other than glome
125 C, and elution from columns with immobilized cystatin C oligomers, oligomer-specific antibodies were
126 .002), and GFR-estimating equations based on cystatin C only.
127                                 In addition, cystatin C participated in the control of extracellular
128 ons, little is known about the regulation of cystatin C production, dimerization, and secretion.
129 of cystatin C under the control of the mouse cystatin C promoter were unable to generate offspring, s
130 mo Diet and Cancer study (MDC) into baseline cystatin C quintiles (n=4757).
131 ation coefficient, serum creatinine-to-serum cystatin C ratio was found to be the best performer in t
132 ient increase in serum creatinine, but serum cystatin C remained stable.
133 t this effect is mediated via an increase in cystatin C secretion.
134                       beta trace protein and cystatin C seem to provide more consistent prognostic in
135 ss or diet), or interference with the assay, cystatin C should be measured and estimated GFR should b
136 ciated with mortality when assessed by serum cystatin C than by creatinine.
137 , these results suggest that the addition of cystatin C to creatinine to estimate GFR may improve ide
138                    Adding the measurement of cystatin C to that of serum creatinine to determine the
139 L68Q) that express the human L68Q variant of cystatin C under the control of the mouse cystatin C pro
140 down-regulated in cell homogenates following cystatin C uptake.
141  hereditary cystatin C amyloid angiopathy, a cystatin C variant is deposited in arterial walls and ca
142                                              Cystatin C warrants further investigation as a more mean
143 ne eGFR was 54+/-20 mL/min per 1.73 m2, mean cystatin C was 11.2 (7.7-16.2) mg/L, and median plasma N
144                             Concurrent serum cystatin C was assayed in banked serum samples.
145                                     Baseline cystatin C was associated with higher carotid intima-med
146                                          Log cystatin C was directly associated with PASP (adjusted b
147 In contrast, the cysteine protease inhibitor cystatin C was expressed only in tubules.
148 ysis adjusted for age, sex, and comorbidity, cystatin C was near-linearly associated with increased m
149                           A causal effect of cystatin C was not detected for any individual component
150                  Although mRNA expression of cystatin C was stable, its secretion, which was inhibite
151 legumain inhibitors, cystatin C, E/M, and F, cystatin C was the one mainly produced.
152 ge glomerular filtration rate estimated from cystatin C well matched follow-up chronic kidney disease
153 mated glomerular filtration rate (eGFR), and cystatin C were assessed in 562 patients with heart fail
154 ardized measurements of serum creatinine and cystatin C were available.
155 ng; urinary albumin-to-creatinine ratio; and cystatin C were evaluated at study baseline.
156                                    Levels of cystatin C were higher in the Tg2576 conditioned medium
157                          Several variants of cystatin C were identified and quantified, while none we
158  kidney disease and when both creatinine and cystatin C were used to calculate the eGFR.
159 ration equation, the eGFR was estimated from cystatin C with all available samples per participant ex
160  extent comparable with the W106F variant of cystatin C with optimal uptake properties and resulting
161                                Reductions in cystatin C with statin therapy correlate with reductions
162 ed vesicular co-localization of internalized cystatin C with the lysosomal marker proteins cathepsin
163  the legumain binding region (N39K- and N39A-cystatin C) decreased the internalization and (R24A,R25A
164 L9G,V10G)-, (R8G,L9G,V10G,W106G)-, and W106G-cystatin C) were internalized to a very low extent compa
165 binding protein, urinary interleukin-18, and cystatin C) were measured in 1,635 unselected emergency
166  markers of filtration (serum creatinine and cystatin C).
167 ment (R(2) = 0.989 for CRP; R(2) = 0.939 for cystatin C).
168 l, 0.8-4.1] per standard deviation change in cystatin C).
169 ct to limits of detection (CRP, 0.10 mug/mL; cystatin C, 0.003 mug/mL) and coefficients of variation
170 he extracellular cysteine protease inhibitor cystatin C, 12 variants of the protein were produced and
171 nd coefficients of variation (CRP, 2.4-7.0%; cystatin C, 3.0-8.9%).
172 al serum potassium levels and measurement of cystatin C, a non-creatinine measure of kidney function.
173 od gas, inflammatory cytokine concentration, cystatin C, and alanine aminotransferase.
174  immunosorption, using immobilized monomeric cystatin C, and elution from columns with immobilized cy
175 Four markers (albumin, beta-2-microglobulin, cystatin C, and osteopontin) were undetectable in most A
176 isease Epidemiology Collaboration creatinine-cystatin C, and urate and high-sensitivity C-reactive pr
177  with increased aortic pulsed wave velocity, cystatin C, and urinary albumin-to-creatinine ratio.
178 fication improvement with the measurement of cystatin C, as compared with creatinine, was 0.23 (95% c
179 FR to a higher value with the measurement of cystatin C, as compared with creatinine, was associated
180 nt variable for kidney function (creatinine, cystatin C, beta2-microglobulin).
181                                        Serum cystatin C, by itself or as a part of an estimated GFR,
182 s, and of the potential legumain inhibitors, cystatin C, E/M, and F, cystatin C was the one mainly pr
183                                    Vimentin, cystatin C, galectin-1, IGFBP-7, and secreted protein, a
184 t and confirmed an increased uptake of W106F-cystatin C, in PC3 cells.
185 of GFR-estimating equations with and without cystatin C, including the modification of diet in renal
186                        Relationships between cystatin C, kidney function, and cardiovascular risk in
187 allel with Elmo1, as do the plasma levels of cystatin C, lipid peroxides, and TGFbeta1, and erythrocy
188 ed GFR, the formula with both creatinine and cystatin C, namely, CKD-epidemiology cr-cys, outperforme
189                  Serum levels of creatinine, cystatin C, or beta trace protein allow estimation of GF
190 lternative biomarkers (haematocrit, cTnI-hs, cystatin C, or creatinine clearance) also outperformed t
191 not increase albuminuria, proteinuria, serum cystatin C, or serum creatinine levels in TxNIP(-/-) mic
192  plasma biomarkers of renal injury including Cystatin C, Osteopontin, Tissue Inhibitor of Metalloprot
193 renal function, C-reactive protein (CRP) and cystatin C, respectively.
194 ith increases in endothelin-1 and creatinine/cystatin C, respectively.
195 ly by iothalamate and creatinine (eGFRcr) or cystatin C, respectively.
196                Two variants, W106F- and K75A-cystatin C, showed that the internalization can be posit
197 ation, we use redox experiments of monomeric cystatin C, stabilized against domain swapping by an int
198 atients had lower levels of cardiotrophin-1, cystatin C, syndecan-4, and N terminal-probrain natriure
199 inar-specific markers-namely, alpha-amylase, cystatin C, TMEM16A, and NKCC1.
200  neutrophil gelatinase-associated lipocalin, cystatin C, trefoil factor 3, tissue inhibitor of metall
201             A secreted factor, identified as cystatin C, was found to be responsible for this effect.
202 eded in a number of assays, such as that for cystatin C, where a 1.5-fold increase in concentration m
203 id not provide evidence for a causal role of cystatin C, with a causal relative risk for CVD of 1.00
204 terminal pro-B-type natriuretic peptide, and cystatin C, with longer QRS interval, with lower heart r
205 utrophil gelatinase-associated lipocalin and cystatin C, with poorer survival.
206 ecreased the internalization and (R24A,R25A)-cystatin C, with substitutions of charged residues not i
207 mination of renal function by creatinine and cystatin C-based eGFR revealed decreasing eGFRs in the d
208 (2) of body-surface area was higher with the cystatin C-based eGFR than with the creatinine-based eGF
209 s were consistent for creatinine-based eGFR, cystatin C-based eGFR, and UACR.
210 tly associated with childhood kidney volume, cystatin C-based eGFR, or the risk of microalbuminuria.
211              Kidney function was measured by cystatin C-based estimated glomerular filtration rate (e
212             One of 3 CKD stages diagnosed by cystatin c-based formulas was incorrect, with both overe
213       We compared 51 creatinine-based and/or cystatin c-based formulas with a gold standard (iohexol
214 e-based formulas: approximately 0.70 and for cystatin c-based formulas: approximately 0.85).
215 012) was superior to previous creatinine- or cystatin C-based GFR equations.
216 , and previously reported creatinine- and/or cystatin C-based GFR-estimating equations.
217 lable creatinine at baseline (n=17 951), and cystatin C-based glomerular filtration rate was estimate
218 our knowledge, no previous studies have used cystatin C-based measures of the estimated glomerular fi
219 IS1: creatinine-based; BIS2: creatinine- and cystatin C-based) with other estimating equations and de
220 0% (creatinine-based) and approximately 50% (cystatin c-based), indicating that 90% of the estimation
221 1 promotes fibrosis by driving the effective cystatin C-dependent inhibition of extracellular matrix-
222 ) in young and middle-aged adults who have a cystatin C-derived estimated glomerular filtration rate
223 D) in children, such as creatinine level and cystatin C-derived estimated glomerular filtration rate
224  data for amyloids from either cystatin B or cystatin C.
225 rer prognosis within cohorts of high and low cystatin C.
226  cells (DC) are the predominant producers of cystatin C.
227  established renal function indices eGFR and cystatin C.
228 rmined by longitudinal measurements of serum cystatin C.
229 tory activity or amyloidogenic properties of cystatin C.
230 ar filtration rate (GFR), estimated GFR, and cystatin C.
231 a traditional sandwich immunoassay for serum cystatin C.
232 han when cells were incubated with wild-type cystatin C.
233 rovement in reclassification with the use of cystatin C.
234 s illustrated by incubating cells with W106F-cystatin C.
235 terminal pro-B type natriuretic peptide, and cystatin C.
236 ylarginine, high-sensitivity troponin T, and cystatin C.
237 for legumain is 100-fold higher than that of cystatin C.
238 equation based on both plasma creatinine and cystatin C.
239  are never labelled with anti-TDP-43 or anti-cystatin C.
240 explaining 2.8% of the observed variation in cystatin C.
241 omarkers (haemoglobin, cTn-hs, and GDF-15 or cystatin C/CKD-EPI) was internally and externally valida
242 factors (relative risk: 1.82 per doubling of cystatin C; 95% confidence interval [CI]: 1.56 to 2.13;
243  we evaluate endogenous cathepsin inhibitors cystatins C and B.
244 tive protein, urinary albumin excretion, and cystatin-C had similar risk for new-onset HF between bot
245 ulative urine volume and the change in serum cystatin-C in 72 hours.
246 -treated groups had a 35% reduction in serum cystatin-C levels and reduced crescent numbers compared
247 n factor 15), GAL-3 (galectin-3), and Cys-C (cystatin-C) were assessed before TAVR and in 100 sex-mat
248 y cardiac troponin T), renal (creatinine and cystatin-C), and hepatic (aspartate transaminase and ala
249 sC5b-9) and renal injury markers (clusterin, cystatin-C, beta2-microglobulin, and liver fatty acid bi
250 , galectin-3, midregional proadrenomedullin, cystatin-C, interleukin-6, procalcitonin, and others.
251                Except for a modest effect of cystatin-C, no biomarker was associated with increased r
252      We further assessed the impact of using cystatin-C-based eGFR in risk prediction equations for C
253  and international guidelines recommend that cystatin-C-based estimates of GFR be used to confirm or
254 measurement method of renal function such as cystatin-C-derived or directly measured GFR.
255  proteinuria, and a 6-fold increase in serum cystatin-C.
256 ctive treatment's effect and EF on change in cystatin-C.
257 he control group; Chromogranin-A[rs9658644], Cystatin-C[rs2424577] and Vitamin K-Dependent Protein S[
258                      Moreover, we identified cystatin CC9 as a novel compatibility factor that suppre
259 ts indicated that a gene encoding a putative cystatin (CC9) is induced upon penetration by U. maydis
260                                     However, cystatin clearance, estimated GFR, and hemoglobin levels
261 m tuberosum) multicystatin (PMC) is a unique cystatin composed of eight repeating units, each capable
262 sistently, transcriptomic analysis show that cystatin D alters gene expression, including that of gen
263                                  Strikingly, cystatin D has been found to inhibit proliferation, migr
264 ese results support an unanticipated role of cystatin D in the cell nucleus, controlling the transcri
265                                              Cystatin D is an inhibitor of lysosomal and secreted cys
266    Here, we demonstrate that a proportion of cystatin D locates within the cell nucleus at specific t
267 hermore, using cytokine arrays we found that cystatin D reduces the secretion of several protumor cyt
268 ied 292 proteins differentially expressed in cystatin D-expressing cells involved in cell adhesion, c
269 of the crystalline form but also exposure of cystatin domains for inhibition of cysteine proteases.
270 verse relationship between the expression of cystatin E/M and cathepsin L and a direct relationship b
271                                        Thus, cystatin E/M appears to be a good candidate to efficient
272 nd a direct relationship between the loss of cystatin E/M expression and nuclear expression of NF-kap
273 cline in drinking water, confirming that the cystatin E/M gene is a tumor suppressor gene.
274            We and others have shown that the cystatin E/M gene is inactivated in primary human tumors
275                       Using plasmid-directed cystatin E/M gene overexpression, a lentivirus-mediated
276 or alpha (TNF-alpha), confirming the role of cystatin E/M in the regulation of the NF-kappaB signalin
277 take of cystatin C and the related inhibitor cystatin E/M occur in melanoma cell lines and to evaluat
278                We therefore propose that the cystatin E/M suppressor gene plays an important role in
279                                              Cystatin E/M was internalized as well but at a modest ra
280                    We have demonstrated that cystatin F (CF) is a critical survival factor for eosino
281 ndosomal/lysosomal cathepsin inhibitor named Cystatin F.
282 ted from pig leukocytes and belonging to the cystatin family of cysteine protease inhibitors.
283                   Similarly, down-regulating cystatin Icy-2, one of the proteinaceous inhibitors of t
284 nd medical applications of several sugarcane cystatins, including CaneCPI-1, CaneCPI-2, CaneCPI-3, an
285                   However, human recombinant cystatin is very expensive, and alternatives to its use
286 ts in the industrial process of lysozyme and cystatin isolation from egg white, and (ii) evaluate the
287 , determined at 1.93 A resolution, shows the cystatin-like fold and is highly similar to the structur
288 lecular interaction site on HRG, possesses a cystatin-like fold composed of a 5-stranded antiparallel
289                PMC is a composite of several cystatins linked by trypsin-sensitive (serine protease)
290 be positively affected by engineering of the cystatin molecule.
291 rt the characterization of a novel sugarcane cystatin, named CaneCPI-5.
292 Under conditions that favour fibrillisation, cystatins populate stable 3D domain-swapped dimers both
293 dundant cathepsins, inhibited by Ca074Me and cystatins, promote pro-IL-1beta synthesis, and to our kn
294                         In this respect, the cystatin scaffold represents an ancestral structural pla
295 etic non-antibody capture protein based on a cystatin scaffold that displays high affinity for human
296   Specifically, acidic proline-rich protein, cystatin, statherin and protein S100-A9 proteins compete
297 er-promoting processes might be controled by cystatin uptake.
298 lation of intracellular enzyme activity by a cystatin variant selected from uptake properties was ill
299                                         This cystatin was efficiently expressed in Escherichia coli,
300 e derived from ovalbumin, ovotransferrin and cystatin were isolated from the most active fractions.

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