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1 -methoxy-, 2-methoxy-, 4,4'-dimethyl-, and 4-chloromethyl-).
2                         2-Chloromethyl and 3-chloromethyl-1,6-methano[10]annulene systems solvolyze i
3 cleaved DNA strand is readily alkylated by 7-chloromethyl 10,11-methylenedioxy CPT; (ii) CPT generall
4          We demonstrate that 7-CM-EDO-CPT (7-chloromethyl-10,11-ethylenedioxy-camptothecin) also indu
5  alkylating camptothecin (CPT) derivative, 7-chloromethyl-10,11-methylenedioxy-camptothecin (7-CM-MDO
6 Alkylation of the top1 cleavage complex by 7-chloromethyl-10,11-methylenedioxycamptothecin (7-ClMe-MD
7 ethylenedioxycamptothecin, 20(S)-glycinate-7-chloromethyl-10,11-methylenedioxycamptothecin, and CPT-1
8 rified beta-tubulin that had reacted with 3-(chloromethyl-[14C] Carbonyl)-3- demethylthiocolchicine (
9   This beta-tubulin that had reacted with 3-(chloromethyl-[14C]carbonyl)- 3-demethythiocolchicine ([1
10 2S,5R)-(-)-menthoxymethylimidazole as amine, chloromethyl (1R,2S,5R)-(-)-menthyl ether as quaternizat
11             In the second method, imidazole, chloromethyl (1R,2S,5R)-(-)-menthyl ether, and DMF are u
12      Reaction of Meldrum's acid with 3,4-bis(chloromethyl)-2,5-dimethylthiophene (1) or 3,4-bis(bromo
13 ch mel were first pre-labeled with 5-(and-6)-chloromethyl-2',7'-dichlorodihydro-fluorescein diacetate
14  microscopy with the fluorescent probe 5',6'-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate
15 of ROS in HRECs was examined using 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate
16 ectively, as derived from the dyes 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate
17 en species were assessed using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate
18 essed by measuring fluorescence of 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate,
19 was detected by the oxidation of 5- (and -6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate,
20 S levels were measured by using the 5- and 6-chloromethyl-2',7'-dichlorodihydrofluorescence diacetate
21 by using dihydroethidium assay and 5-(and 6)-chloromethyl-2',7'-dichlorodihydrofluorescence diacetate
22 ted with the fluorigenic substrate 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescin diacetate,
23                    Among tested compounds 4'-chloromethyl-2'-deoxy-2'-fluorocytidine (2c) exhibited t
24 ion of methylenebisacetamide with 3-chloro-2-chloromethyl-2-propene to provide 5-exomethylene-1, 3-di
25 n the pseudo-first-order formation of (Z)-2-(chloromethyl)-3-(2-hydroxyphenyl)-2-propenoic acid.
26 actions of the bifunctional allylstannane 2-(chloromethyl)-3-(tributylstannyl)propene with aldehydes
27 ntraction to (2S,3R,4S,5S,1'R)-N(1)-benzyl-2-chloromethyl-3-benzyloxy-4,5-epoxypiperidine followed by
28 give the 4-(chloromethyl)benzoyl ester of 4-(chloromethyl)-4'-hydroxybenzophenone followed by reactio
29 the presence of an electrophilic reagent, 1-(chloromethyl)-4-fluoro-1,4-diazoniabicyclo[2.2.2]octane
30 coupling of the triamines 4a-d with 2, 6-bis(chloromethyl)-4-methylphenol 5 and results in the format
31  monocarbonyl compounds, with Selectfluor (1-chloromethyl-4-fluoro-1,4-diazoniabicyclo[2.2.2]octane b
32 ul analogues (MXY, in general): (3-chloro-4-(chloromethyl)-5-hydroxy-2(5H)-furanone -CMCF- and 3-chlo
33 y, a conjugate molecule [polyamide 1-CBI (1-(chloromethyl)-5-hydroxyl-1,2-dihydro-3H-benz[e]indole) c
34 fords a conjugate 1-CBI (polyamide 1-CBI (1-(chloromethyl)-5-hydroxyl-1,2-dihydro-3H-benz[e]indole) c
35                                            6-Chloromethyl-6-methylfulvene, also a primary, allylic ha
36 lfonyl-THIQ (R-13) and both enantiomers of 3-chloromethyl-7-nitro-THIQ (R- and S-30) are the most sel
37  of 3-fluoromethyl-, 3-hydroxymethyl-, and 3-chloromethyl-7-substituted-1,2,3,4-tetrahydroisoquinolin
38  rhomboid protease inhibitor N-p-Tosyl-l-Phe chloromethyl abolishes the induction of AOX1a upon antim
39                                              Chloromethyl addition was achieved under both the tin-fr
40                                  Undisclosed chloromethyl alkanoates (chloromethyl propanoate, pentan
41 chloromethylcarbinols for the preparation of chloromethyl-alpha-diketones, trichloromethylated dihydr
42                                            2-Chloromethyl and 3-chloromethyl-1,6-methano[10]annulene
43                                 Iodomethyl-, chloromethyl-, and fluoromethyldimethylsulfonium salts,
44  sulfonium ylide 4, and sulfonyl-substituted chloromethyl anion 5.
45 tion of 3-methylbenzoate affording methyl 3-(chloromethyl)benzoate, which is an important building bl
46 y a synthetic route involving reaction of 4-(chloromethyl)benzoic anhydride with phenol in polyphosph
47 phenol in polyphosphoric acid to give the 4-(chloromethyl)benzoyl ester of 4-(chloromethyl)-4'-hydrox
48 with a fluorescent vital dye [(5-(and-6)-((4-chloromethyl)benzoyl)amino)tetramethylrhodamine], which
49       The classical antifolate 7 utilized 4-(chloromethyl)benzoyl-l-glutamic acid diethyl ester (17)
50 e at m1 receptors, approximately 3-fold by N-chloromethyl brucine at m3 receptors, and approximately
51 he subtype-selective allosteric effects of N-chloromethyl brucine on M2 and M3 receptors were shown t
52                    The enhancing action of N-chloromethyl brucine on neurogenically released ACh bind
53                   Neutral cooperativity of N-chloromethyl brucine with ACh on M4 receptor function wa
54 tudies, it has been reported that brucine, N-chloromethyl brucine, and brucine N-oxide increased the
55 ric site that binds strychnine (and probably chloromethyl brucine, another allosteric enhancer) there
56 plays selectivity for the carbonyl carbon of chloromethyl carbonyl electrophiles.
57 actions conducted at 0 degrees C afforded 2-(chloromethyl)cinnamic acid derivatives as the major prod
58 -2) with the fluorogenic substrate 7-amino-4-chloromethyl coumarin (CMAC).
59 ogenic rGSTT2-2-specific substrate 7-amino-4-chloromethyl coumarin led to the isolation of active var
60 ed in refluxing acetic acid, however, the 3-(chloromethyl)coumarin derivatives are the sole products.
61  the major products and the corresponding 3-(chloromethyl)coumarin derivatives as the minor products.
62                                          The chloromethyl derivative 3 readily decomposes on warming
63  fluorometrically using propidium iodide and chloromethyl dihydrodichlorofluorescein, respectively.
64 5ClCH2(CH3)2SiOSi(CH3)2+ formed from 1,3-bis(chloromethyl)disiloxane upon an F-SAM surface, (iv) surf
65  synthetic methodology is efficient and uses chloromethyl ethers derived from the chirons diethyl (3S
66 wed by a Wittig reaction with 2,4-diamino-5-(chloromethyl)furo[2,3-d]pyrimidine (6), catalytic hydrog
67 sized by a Wittig reaction of 2,4-diamino-5-(chloromethyl)furo[2,3-d]pyrimidine with ethyl 4-acetylbe
68  nucleophilic displacement of 2,4-diamino-5-(chloromethyl)furo[2,3-d]pyrimidine(2) with the appropria
69  highly reactive, genotoxic intermediate, S-(chloromethyl)glutathione (GS-CH(2)Cl).
70 oate (14), which was elaborated to the alpha-chloromethyl ketone (8) followed by condensation with 2,
71 ltransferase (LRAT) with 10-N-acetamidodecyl chloromethyl ketone (AcDCMK) or cellular retinol-binding
72             The hemiketal hydroxyl groups in chloromethyl ketone (cmk) complexes of trypsin and chymo
73 hloride (AEBSF) and decanoyl-Arg-Arg-Leu-Leu-chloromethyl ketone (dec-RRLL-cmk), inhibitors of SKI-1
74 ing the membrane-permeable synthetic peptide chloromethyl ketone (decanoyl-RVKR-CMK) blocked regulate
75 the active site inhibitor dansyl-Glu-Gly-Arg-chloromethyl ketone (DEGR-CMK) in a slow reaction.
76 he synthesis of paclitaxel (PTX)-Phe-Phe-Arg-chloromethyl ketone (FFR-ck), followed by coupling with
77 The optimized inhibitor peptide dPhe-Pro-Arg chloromethyl ketone (PPACK) was used to simulate the sub
78 y treatment of the enzyme with D-Phe-Pro-Arg-chloromethyl ketone (PPACK), a reagent that irreversibly
79 ride (PMSF) (100%), N-alpha-p-tosyl-l-lysine chloromethyl ketone (TLCK) (85.4%), benzamidine (80.2%),
80 ted by the protease inhibitor tosyl-l-lysine chloromethyl ketone (TLCK) (P < 0.05).
81 ther treatment with N alpha-p-tosyl-L-lysine chloromethyl ketone (TLCK) and dithiothreitol was perfor
82 lso was inhibited by Nalpha-p-tosyl-L-lysine chloromethyl ketone (TLCK) and, to a lesser extent, H-D-
83 e protease inhibitor Nalpha-p-tosyl-L-lysine chloromethyl ketone (TLCK) blocked its effects on cultur
84 inhibitors ZnCl2 and Nalpha-p-tosyl-l-lysine chloromethyl ketone (TLCK) exhibited dose-dependent inhi
85 hloromethyl ketone (TPCK) and tosyl-L-lysine chloromethyl ketone (TLCK) modified the HPV type 18 E7 p
86 proteasome inhibitor Nalpha-p-tosyl-L-lysine chloromethyl ketone (TLCK) or by infection with rAd-Ikap
87 revented apoptosis, whereas N-tosyl-L-lysine chloromethyl ketone (TLCK), Ac-Leu-Leu-L-norleucinal, Ac
88  protease inhibitor, Nalpha-P-tosyl-L-lysine chloromethyl ketone (TLCK), and a proteasome complex (26
89 ly blocked apoptosis, but N-p-tosyl-L-lysine chloromethyl ketone (TLCK), another serine protease inhi
90  serine protease inhibitor, N-tosyl-L-lysine chloromethyl ketone (TLCK), dramatically enhances Fas-me
91 seen with active and Nalpha-p-tosyl-L-lysine chloromethyl ketone (TLCK)-inactivated HRgpA, indicating
92 e chloromethyl ketone (TPCK) and tosyllysine chloromethyl ketone (TLCK).
93  and by exposure to N alpha-p-tosyl-L-lysine chloromethyl ketone (TLCK).
94 rtially inhibited by N-tosyl-l-phenylalanine chloromethyl ketone (TPCK) (10.3%), ethylendiaminetetraa
95 serine protease inhibitors, N-tosyl-L-phenyl chloromethyl ketone (TPCK) and 3,4-dichloroisocoumarin (
96 ne protease inhibitors tosyl-L-phenylalanine chloromethyl ketone (TPCK) and tosyl-L-lysine chlorometh
97 erine protease inhibitors tosylphenylalanine chloromethyl ketone (TPCK) and tosyllysine chloromethyl
98 tease inhibitor L-1-tosylamido-2-phenylethyl chloromethyl ketone (TPCK) did not inhibit the sensitiza
99 e protease inhibitor N-tosyl-L-phenylalanine chloromethyl ketone (TPCK) effectively blocked apoptosis
100 tive effects of N-alpha-tosyl-l-phenylalanyl chloromethyl ketone (TPCK) have been known for more than
101 ease inhibitor N-alpha-tosyl-L-phenylalanine chloromethyl ketone (TPCK) prevents UV activation of HIV
102 hymotryptic inhibitor N-tosyl-L-phenylalanyl-chloromethyl ketone (TPCK) suppressed DNA fragmentation
103  WEH1 231 cells with N-tosyl-L-phenylalanine chloromethyl ketone (TPCK), a protease inhibitor which p
104 B inhibitor, or l-1-tosylamido-2-phenylethyl chloromethyl ketone (TPCK), a serine protease inhibitor
105 e infection to l-(tosylamido-2-phenyl) ethyl chloromethyl ketone (TPCK), a serine-cysteine protease i
106 itors, dexamethasone and n-tosylphenyalanine chloromethyl ketone (TPCK), abolishes constitutive RelA
107  were inactivated by N-tosyl-L-phenylalanine chloromethyl ketone (TPCK), an inhibitor of chymotrypsin
108 NF-kappa B, SN50 and N-tosyl-l-phenylalanine chloromethyl ketone (TPCK), blocks TNF-induced Akt activ
109 e protease inhibitor N-tosyl-L-phenylalanine chloromethyl ketone (TPCK), which blocks the normally ra
110 e protease inhibitor N-Tosyl-L-Phenylalanine Chloromethyl Ketone (TPCK).
111 ine protease inhibitor tosyl-L-phenylalanine chloromethyl ketone (TPCK).
112  to a lesser extent, H-D-Tyr-L-Pro-L-arginyl chloromethyl ketone (YPRCK) and was relatively insensiti
113 roteinase inhibitor N-alpha-p-tosyl-L-lysine chloromethyl ketone and also by a caspase inhibitor.
114                 The factor Xa inhibitor DEGR-chloromethyl ketone and an antibody to factor X inhibite
115 ysis are inhibited by acetyl-Tyr-Val-Ala-Asp chloromethyl ketone and CrmA, specific inhibitors of ICE
116 protease inhibitors N-tosyl-L -phenylalanine chloromethyl ketone and N-acetyl-L -leucinyl-L -leucinyl
117 hrough inhibition studies with both peptidyl chloromethyl ketone and organophosphate inhibitors.
118  was corroborated by inhibition studies with chloromethyl ketone and organophosphonate inhibitors.
119 ors of this pathway, N-tosyl-l-phenylalanine chloromethyl ketone and pyrrolidine dithiocarbamate, abr
120 aB inhibitors, e.g., N-tosyl-l-phenylalanine chloromethyl ketone and SN50, a result that is consisten
121 licated in apoptosis, only tosylphenylalanyl chloromethyl ketone and the nuclear scaffold protease in
122 zyme activity in the presence of N-p-tosyl-L-chloromethyl ketone and the partial inhibition of enzyme
123 tone, ALLN, and Nalpha-tosyl-L-phenylalanine chloromethyl ketone and was relatively unaffected by lac
124 proteasome inhibitor N-tosyl-L-phenylalanine chloromethyl ketone blocked expression of TF mRNA and ac
125 caspase-1 activity by acetyl-Tyr-Val-Ala-Asp-chloromethyl ketone blocks macrophage cytotoxicity, and
126        The co-crystal structure revealed the chloromethyl ketone bound to the N-terminal nucleophile
127 e and to the inhibitor-derived oxyanion in a chloromethyl ketone complex, observations that strongly
128 onyl)-L-Leu]-agmatine (E-64) and tosyl-L-Lys chloromethyl ketone did not inhibit PEPase activity.
129  stabilization of FXa(I16L) with Glu-Gly-Arg-chloromethyl ketone fully rescued FVa binding.
130 onvertase inhibitor decanoyl-Arg-Val-Lys-Arg-chloromethyl ketone had greater versican-cleaving activi
131 sence or absence of decanoyl-Arg-Val-Lys-Arg-chloromethyl ketone in COS-7 cells expressing Phex and F
132  transitions, we designed a pantetheine-like chloromethyl ketone inactivator and co-crystallized it w
133 hibitor of trypsin, N-alpha-p-tosyl-L-lysine chloromethyl ketone inhibited 99.67% activity.
134                                  Tosyl-lysyl chloromethyl ketone inhibited the trypsin-like protease
135                                D-Phe-Pro-Arg-chloromethyl ketone inhibition at the thrombin active si
136  was blocked by active site-directed peptide chloromethyl ketone inhibitors; (ii) the kinetics of com
137 zothiazole group linked to the D-Phe-Pro-Arg chloromethyl ketone motif.
138 labeling with dansyl-glutamyl-glycyl-arginyl chloromethyl ketone or immunoblot analysis showed no det
139 n S and a triazole inhibitor incorporating a chloromethyl ketone pharmacophore guided the design of t
140 midine-FVIIa/sTF crystals with d-Phe-Pro-Arg-chloromethyl ketone results in benzamidine displacement,
141    The PC inhibitor decanoyl-Arg-Val-Lys-Arg-chloromethyl ketone significantly suppressed FLAG-pro-GX
142 sing Xa modified with a fluorescent peptidyl chloromethyl ketone to irreversibly occlude the active s
143 nding of the covalent inhibitor dPhe-Pro-Arg chloromethyl ketone to the active site serine, as well a
144 ed by 1 mM N-methoxysuccinyl-Ala-Ala-Pro-Val chloromethyl ketone when it was present during activatio
145 ase inhibitors TLCK (Nalpha-p-tosyl-l-lysine chloromethyl ketone) and E-64 [l-trans-epoxysuccinyl-leu
146 s inhibited by TLCK (Nalpha-p-tosyl-L-lysine chloromethyl ketone) and iodoacetamide.
147 inactivated by TLCK (Nalpha-p-tosyl-L-lysine chloromethyl ketone) and proteinase K treatment.
148 ffold multicatalytic proteinase (Ala-Pro-Phe chloromethyl ketone) block the degradation of lamin B1 t
149 -kappaB inhibitor (N-p-Tosyl-L-phenylalanine chloromethyl ketone) that restored PGC-1alpha recovery a
150 nhibited by TPCK (tolylsullonyl phenylalanyl chloromethyl ketone), PMSF (phenylmethylsulfonyl fluorid
151 ase inhibitor TLCK (N alpha-p-tosyl-L-lysine chloromethyl ketone), pronase, or proteinase K, suggesti
152 tion of phenylalanine-phenylalanine-arginine chloromethyl ketone, (FFRck) followed by coupling with t
153                              Tyr-Val-Ala-Asp-chloromethyl ketone, a caspase-1 inhibitor, prevented AT
154  more specifically N-p-tosyl-L-phenylalanine chloromethyl ketone, a chymotrypsin-like proteinase inhi
155 ed by N-acetyltyrosinylvalinylalanylaspartyl chloromethyl ketone, a peptide inhibitor of interleukin-
156 ccinyl-alanine-alanine-proline-valine (AAPV) chloromethyl ketone, a specific neutrophil elastase inhi
157 l prothrombin derivatives with D-Phe-Pro-Arg-chloromethyl ketone, analogous to irreversible binding o
158 loromethyl ketone, N(alpha)-p-tosyl-L-lysine chloromethyl ketone, and N-(N(alpha)-benzyloxycarbonylph
159  could be blocked by N-tosyl-L-phenylalanine chloromethyl ketone, calpeptin, and pyrrolidine dithioca
160 arbonyl-glycine-leucine-phenylalanine (ZGLF) chloromethyl ketone, had no effect.
161 irudin and D-phenylalanyl-L-prolyl-L-arginyl chloromethyl ketone, indicating that the effect of c7E3
162 itor of serine proteases, Na-p-Tosyl-L-lysyl-chloromethyl ketone, inhibited radiation-induced apoptos
163 socoumarin, N(alpha)-p-tosyl-L-phenylalanine chloromethyl ketone, N(alpha)-p-tosyl-L-lysine chloromet
164 se inhibitor N alpha-L-tosyl-L-phenylalanine chloromethyl ketone, suggesting that a nuclear factor-ka
165 tick-anticoagulant-peptide and D-Glu-Gly-Arg-chloromethyl ketone, the latter two being specific inhib
166 proteinase inhibitor and dec-Arg-Val-Lys-Arg-chloromethyl ketone, two specific furin inhibitors, bloc
167  interactions, we crystallized d-Phe-Pro-Arg-chloromethyl ketone-inhibited human thrombin in complex
168 ts by an endogenous decanoyl-Arg-Val-Lys-Arg-chloromethyl ketone-sensitive furin-type convertase.
169 luoride and N(alpha)-p-tosyl-L-phenylalanine chloromethyl ketone.
170  in the presence of N-alpha-p-tosyl-L-lysine chloromethyl ketone.
171  unaffected by lactacystin and N-tosyl lysyl chloromethyl ketone.
172 , tick anticoagulant peptide, or Glu-Gly-Arg-chloromethyl ketone.
173 tor, CrmA, and N-alpha-tosyl-L-phenylalanine chloromethyl ketone.
174 bitor, or d-phenylalanyl-l-prolyl-l-arginine chloromethyl ketone.
175 toichiometrically with the thioester peptide chloromethyl ketone.
176 nt adduct of Chtr with N-p-tosylphenylalanyl chloromethyl ketone.
177 on with phenylalanine-phenylalanine-arginine-chloromethyl ketone.
178 cubation with a caspase-3 inhibitor (Ac-DEVD-chloromethyl-ketone) further attenuated the ultraviolet
179 synthetic inhibitor decanoyl-Arg-Val-Lys-Arg-chloromethyl-ketone, CMK, showed a significant decrease
180 to the active site inhibitor H-d-Phe-Pro-Arg-chloromethyl-ketone, document the conformational changes
181 f sodium tolylsulfinate with bromomethyl- or chloromethyl ketones generates beta-keto sulfones.
182                Biotin derivatives of peptide chloromethyl ketones have ideal properties for specific
183  2-chloroacetamidine is analogous to that of chloromethyl ketones, a set of inhibitors that have foun
184 bitors may be applicable to other tripeptide chloromethyl ketones, and the reagents can be employed f
185 the PBPs were synthesized, including peptide chloromethyl ketones, trifluoromethyl ketones, aldehydes
186 combined with the electron affinity of the 5-chloromethyl-m-xylylene biradical (1.120 +/- 0.059 eV) t
187 benzene, which was generated by CID of the 5-chloromethyl-m-xylylene ion.
188 al(k)Val units were prepared and attached to chloromethyl Merrifield resin via the carboxy terminal.
189  highest affinity and THIQs containing the 3-chloromethyl moiety the least.
190 nversion to a chloride gave 5-substituted 3-(chloromethyl)- or 3-(2-chloroethyl)pyrazoles.
191 nt of acetyl chloride, benzoyl chloride, and chloromethyl oxalate to the 3-position of 4-, 5-, 6-, or
192 ion between tert-butoxycarbonyl alaninal and chloromethyl phenyl sulfone afforded chlorohydrins, whic
193 s to organelles that double-label with 8-(4'-chloromethyl) phenyl-2,3,5,6,11,12,14,15-octahydro-1H,4H
194 hanol, alpha-ionone, 3-methyl-1-indanone, o-(chloromethyl)phenyl sulfoxide, o-(bromomethyl)phenyl sul
195 lf-assembling a densely bonded monolayer of (chloromethyl)-phenylethyltrichlorosilane (CMPES).
196  a novel derivatizing reagent, di-tert-butyl chloromethyl phosphate, resulting in formation of the qu
197 oxides bearing alkyl, alkenyl, aryl, alkoxy, chloromethyl, phthalimido, and acetal functional groups.
198                                      2,2-bis(chloromethyl)propane-1,3-diyltetrakis(2-chloroethyl) bis
199 hexyl) adipate (DEHA)), and one FR (2,2-bis (chloromethyl)-propane-1,3-diyltetrakis(2-chloroethyl) bi
200         Undisclosed chloromethyl alkanoates (chloromethyl propanoate, pentanoate, and octanoate) were
201  nucleophilic displacement of 2,6-diamino-8-(chloromethyl)purine with the appropriate anilines or 2-n
202 tetramethylindo carbocyanine perchlorate, or chloromethyl tetramethylrhodamine.
203 ese 3-fluoromethyl-, 3-hydroxymethyl-, and 3-chloromethyl-THIQs indicates that all of the 3-substitut
204 ese 3-fluoromethyl-, 3-hydroxymethyl-, and 3-chloromethyl-THIQs.
205             Flow cytometry experiments using chloromethyl-X-rosamine and Indo-1 revealed FimH-depende

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