ライフサイエンスコーパス: inactive mutant

1 g conferred activity upon G85R, an otherwise inactive mutant.

2 pe Mps1 transgene but not by a catalytically inactive mutant.

3 as inferred from the use of an enzymatically inactive mutant.

4 cued by wild-type DGKzeta or a catalytically inactive mutant.

5 tutively active M1 mAChR but abolished at an inactive mutant.

6 their intracellular site of action by using inactive mutants.

7 ession of wild-type CaMKK2 but not by kinase-inactive mutants.

8 lleagues in the degradation of catalytically inactive mutant 25S ribosomal RNAS (rRNAs) in mature 60S

9 the structure of wild type and catalytically inactive mutants alone and in complex with DNA.

10 ated by mistranslation of a gene encoding an inactive mutant alpha chain of the Vibrio harveyi enzyme

11 Two catalytically inactive mutants also inhibited LcA activity.

12 erexpressing wild-type p100, but not its GEP-inactive mutants, also consistent with the conclusion th

13 Expression of the catalytically inactive mutants, AMSH(D348A) and UBPY(C786S), caused an

14 Overexpression of an AIP4 catalytically inactive mutant and a mutant that shows poor binding to

15 tro; no interaction was detected between gp8 inactive mutants and wild-type delta or between delta gp

16 d a combination of protease (wild type or an inactive mutant) and portal proteins and overexpressing

17 y structures of the wild-type FP and the two inactive mutants are quite similar, indicating that the

18 , a proportion of both dismutase-active and -inactive mutants are stably bound to spinal cord mitocho

19 ) cells or ARH1(-/-) cells overexpressing an inactive mutant ARH1 protein (ARH1(-/-)+dm) had higher p

20 ted with wild-type A20 or with catalytically inactive mutants as a control.

21 rs, supporting the hypothesis that these two inactive mutants associate directly to function in trans

22 tently, wild-type Aurora A, but not a kinase inactive mutant, becomes autophosphorylated on the regul

23 HAE cells with HE but not the enzymatically inactive mutant blocked hCoV-HKU1 infection.

24 Moreover, expression of TrkA kinase-inactive mutant blocked the activation of Akt and Erk5 i

25 Furthermore, this kinase-inactive mutant blocks the translocation of RPA in a cel

26 ession of guanine nucleotide-exchange factor inactive mutant, but not wild-type, proteins interfered

27 Expression of wild type cPAcP, but not inactive mutant, by cDNA in cPAcP-null LNCaP C-81 cells

28 Phospho-Tyr-731-inactive mutant c-Cbl (Y731F) enhances and phosphomimeti

29 TG2 and the transaminase-inactive mutant C277S-TG2 inhibited a HIF-dependent tran

30 In this work, a catalytically inactive mutant (C84A) of Co(2+)-substituted Bacillus su

31 olamide or coexpression of the catalytically inactive mutant CAIV-V165Y did not suppress CAIV-mediate

32 Inactive mutants can be achieved either by targeting act

33 so interfere with phosphorylation, but these inactive mutants can be phosphorylated when an active fo

34 X2 complexes in vitro, whereas catalytically inactive mutants cannot dephosphorylate Aurora A or resc

35 rdiac TnC (cTnC) or a mixture of cTnC and an inactive mutant cardiac TnC (CBMII TnC).

36 of wild type (WT), but not the catalytically inactive mutant CerS6, increased tumor growth in SCID mi

37 Overexpression of CHIP, but not of the inactive mutant CHIP K30A, induced accumulation of AXL p

38 onversely, overexpression of a catalytically inactive mutant, Clk/STY(K190R), causes retention of hyp

39 The use of a catalytically inactive mutant confirmed these effects to be primarily

40 or its constitutive active form, but not the inactive mutant, converted the Golgi membranes into COPI

41 transport activity with increasing levels of inactive mutant correlated linearly with the fraction of

42 however, can be disrupted by a catalytically inactive mutant D408N gp43 that retains normal affinity

43 We have determined the crystal structure of inactive mutant (D88N) of RecU from Bacillus subtilis in

44 C-SIGN and other C-type lectins, but not the inactive mutant DC-SIGNDelta35, which lacks a cytoplasmi

45 of wild-type RNF4, but not the catalytically inactive mutant, decreased the steady-state levels of Nr

46 n of the influenza virus, wt20, and a fusion-inactive mutant DeltaG1 with dimyristoylphosphatidylchol

47 pe (+/+) TACE but not on those expressing an inactive mutant (DeltaZn/DeltaZn), confirming the role o

48 Ectopic expression of a catalytically inactive mutant did not elicit any of the phenotypes, wh

49 show that the majority of the catalytically inactive mutants did not fold.

50 kappa-Balpha, whereas the three biologically inactive mutants did not induce degradation.

51 The enzymatically inactive mutants differed in their signaling ability.

52 ably expressing CK2alpha or CK2alpha' kinase-inactive mutants, displayed decreased NF-kappaB binding

53 ssion of PKD3 wild type, but not PKD3 kinase-inactive mutant, disrupted the formation of apical inter

54 ver, SHP2 wild type, but not a catalytically inactive mutant, dissociated SOCS1 from ASK1.

55 reas expression of each of the catalytically inactive mutant domains was not.

56 olate are shown to rescue the activity of an inactive mutant, E101A, in the K proton pathway of Rhodo

57 pic expression of wild-type E2F1, but not an inactive mutant E2F1(132E), activated the XRCC1 promoter

58 8 to natural killer cells, whereas the three inactive mutants E42X, K89E, and K89X were unable to com

59 Two structures of the catalytically inactive mutant E72A complexed with Co(2+) and either th

60 The inactive mutant E88A shows increased septal localization

61 4A protease, but not a related catalytically inactive mutant, effectively blocks innate intracellular

62 ss-linked to a functional PLE, but not to an inactive mutant element.

63 wild-type STAMBPL1, but not a catalytically inactive mutant, enhanced Tax-mediated NF-kappaB activat

64 Expression of a Map4k4 kinase-inactive mutant enhances myotube formation, suggesting t

65 itro vacuole fusion, as does a catalytically inactive mutant enolase, suggesting a role for enolase i

66 Incubation of pairs of inactive mutant enzymes led to reconstitution of some fu

67 of HeLa cells expressing wild-type ER and an inactive mutant ERalpha unable to bind estrogen response

68 Intriguingly, Pak1 phosphorylation inactive mutant ESE1-S207A is more unstable than either

69 ell lines expressing either human FAAH or an inactive mutant, FAAH-S241A, were established.

70 defect is specific for DNA molecules because inactive mutants fail to bind a consensus p53 response e

71 IRAK4 kinase-inactive mutant failed to mediate the IL-1R-TLR-induced

72 cytokines with irrelevant specificity and/or inactive mutant Fc domains behaved similarly to tumor-sp

73 Moreover, a kinase-inactive mutant, FLAG-Ki-KSR1(D683A/D700A), which effici

74 pic expression of wild-type CKL6 or a kinase-inactive mutant form induced alterations in cortical mic

75 be restored by expression of a catalytically inactive mutant form of cdk5.

76 lpP and competition between wild-type and an inactive mutant form of ClpP, that this effect on degrad

77 pase A(2) (sPLA(2)), but not a catalytically inactive mutant form of GX sPLA(2), significantly reduce

78 We have determined crystal structures of an inactive mutant form of H. pylori MTAN bound to MTA and

79 we use cell lines expressing a catalytically inactive mutant form of LOX to show that catalytic activ

80 o PTPmu, wild-type PTPmu, or a catalytically inactive mutant form of PTPmu, and homophilic adhesion w

81 ticularly effective activator of ALDH2*2, an inactive mutant form of the enzyme that is found in 40%

82 The wild-type enzyme and its inactive mutant forms were expressed in soybean roots in

83 In contrast, a transcriptionally inactive mutant Foxo1 partially rescues inhibition of C2

84 dystrophin protein production from otherwise inactive mutant genes.

85 The crystal structure of the inactive mutant Glu212-->Gln of this protein has also be

86 acted on both receptors, whereas the kinase-inactive mutant GRK2-D110A/K220R failed to inhibit signa

87 ntaining GTR and wild-type GSAT, addition of inactive mutant GSAT inhibited ALA formation from glutam

88 A 1.85 A resolution crystal structure of the inactive mutant H59N-AaPurE soaked in CAIR showed that p

89 sembled without hA3A or with a catalytically inactive mutant, hA3A/E72Q.

90 However, we now found that the IRAK4 kinase-inactive mutant had the same ability as the wild-type IR

91 Two of the inactive mutants had unusual secondary structures compar

92 yte lysate inhibit translation, while kinase-inactive mutants have no effect.

93 annose, and three cocrystal structures of an inactive mutant (His-124 --> Leu) Gmm bound to substrate

94 ctors containing hPKGIalpha or catalytically inactive mutant hPKGIalphaK390A.

95 ng to increased cell death, whereas protease-inactive mutant HtrA1 failed to result in either the inh

96 module of CbhA (Ig-GH9_CbhA) and that of an inactive mutant Ig-GH9_CbhA(E795Q) in complex with cello

97 Caf1 or overexpressing a Caf1 catalytically inactive mutant impairs deadenylation and mRNA decay.

98 N1-cIDPR forms a complex with CD38 or its inactive mutant in which the catalytic residue Glu-226 i

99 of DBT and its short, long, arrhythmic, and inactive mutants in S2 cells.

100 F (TFIIF) partially restored activity of the inactive mutants in the minimal promoter system, suggest

101 ression of wild-type HIPK2, but not a kinase-inactive mutant, in a glioma cell line conferred a growt

102 genase (17beta-HSD10), but not its catalytic inactive mutant, increased significantly as allopregnano

103 Kinase-inactive mutant IRAK is still phosphorylated in response

104 490A, whereas cells expressing S490D and the inactive mutants K278R and T402A grow exponentially, ind

105 f the trans-dominant negative, catalytically inactive mutant K296R to inhibit PKR activity in neurobl

106 Overexpression of a lipase inactive mutant (K758R), however, failed to induce an in

107 Phosphorylation of an inactive mutant KD was reduced by G-helix substitutions

108 tal structures of the cleaved form and of an inactive mutant lacking the membrane-spanning region.

109 peptidoglycan and report that catalytically inactive mutants lead to defects in colonization that ap

110 Expression of active MTF, but not of an inactive mutant, leads to formylation of methionine atta

111 more, fluorescence studies revealed that the inactive mutants lost their ability to interact with the

112 Interestingly, one of these inactive mutants maintained binding to the exocyst compl

113 rS1 expression, but not by its catalytically inactive mutant, mediated the association and recruitmen

114 els were not significantly altered in kinase-inactive mutant mice.

115 (WT) PTP1B, but not its C215S catalytically inactive mutant mimicked the actions of hSPRY2 on tyrosi

116 Using the catalytically inactive mutant MMP-2EA (the E404A mutant of proMMP-2),

117 F-R beta was attenuated by the catalytically inactive mutant mPLD2-K758R.

118 Wild-type mPLK, but not a kinase-inactive mutant (mPLK-KD), directly phosphorylated full-

119 ression of wild type (WT), but not catalytic inactive mutant (Mut), TET2 in low-TET-expressing cells

120 in COS7 cells overexpressing a catalytically inactive mutant of ADAM17.

121 lytic because the same products form with an inactive mutant of ADAMTS4 (a disintegrin and metallopro

122 Cells expressing a catalytically inactive mutant of AMSH show basal hyperubiquitination,

123 inetics of EGFR fused with the catalytically inactive mutant of AMSH were reversed to normal.

124 We overexpressed an inactive mutant of Atg5 to create an autophagy-deficient

125 the second structure is for a catalytically inactive mutant of BcsZ in complex with the substrate ce

126 n contrast, the wild-type but not the ATPase-inactive mutant of Brg1 suppressed MT-I promoter irrespe

127 Expression of the catalytically inactive mutant of calpain1 reduces the cleavage to enha

128 , while a CerS inhibitor and a catalytically inactive mutant of CerS6 failed to reduce it.

129 A kinase-inactive mutant of CK2alpha was able to block ectopic ax

130 r, we unexpectedly showed, by using a kinase-inactive mutant of CK2alpha, that RAF-MEK inhibitor resi

131 Further, we show that a catalytically inactive mutant of CoaSt6 was unable to enhance Stat6-me

132 Similarly, constitutively inactive mutant of cofilin-1 (Cof1-S3D), known to stabil

133 A catalytically inactive mutant of CypA was also able to inhibit TBSV re

134 rowth phenotype, whereas, coexpression of an inactive mutant of DEF does not.

135 A catalytically inactive mutant of DGAT1 (H426A) blocks the localization

136 Finally, the expression of a catalytically inactive mutant of DUSP5 also tethers ERK2 within the nu

137 We found that the wild type and the inactive mutant of Galphao reduce the Kir2.4 basal curre

138 (+P) was isolated by coexpressing gp5 and an inactive mutant of gp4.

139 larly, and overexpression of a catalytically inactive mutant of GRK2 produced the same effects.

140 Expression of an inactive mutant of HGK also inhibited the anchorage-inde

141 Incorporation of the inactive mutant of hGSTA4-4 (Y212F) in cells by either m

142 ction experiments showed that HN (but not an inactive mutant of HN) also protects intact cells from a

143 2), a close homolog of hVPLA(2), or W31A, an inactive mutant of hVPLA(2), did not affect these respon

144 Overexpression of IKKbeta-KM, a kinase inactive mutant of IKKbeta, blocked NF-kappaB activation

145 cifically by coexpression of a catalytically inactive mutant of IKKepsilon; and 3) mutants of IRF3, e

146 ely blocked by expression of a catalytically inactive mutant of Janus kinase 3 (Jak3), and increased

147 essed by ectopic expression of catalytically inactive mutant of JNK kinase 2 (JNKK2(AA)).

148 ted by ectopic expression of a catalytically inactive mutant of JNK kinase 2 and RNA interference of

149 was abolished in mitochondria expressing an inactive mutant of Kir6.2.

150 In contrast, NRP1 binding of an inactive mutant of LD22-4 was substantially reduced.

151 s) as well as controls using a catalytically inactive mutant of LT and vesicles lacking LT.

152 ivation of JNK that is inhibited by a kinase-inactive mutant of MEKK4, MEKK4K1361R.

153 ribed crystal structure of a metacaspase, an inactive mutant of metacaspase 2 (MCA2) from Trypanosoma

154 xpressing both wild type and a catalytically inactive mutant of MKP-1 (MKP-1/CS) were constructed to

155 MMP markedly enhanced activation, whereas an inactive mutant of MT4-MMP was ineffective.

156 e, and to solve the solution structure of an inactive mutant of MVL in complex with this unexpected s

157 However, catalytically inactive mutant of nsp4 abolished its ability to cleave

158 at were cotransfected with p12 and a caspase inactive mutant of p17.

159 Unexpectedly, we find that a catalytically inactive mutant of PBP 2B supports cell division, but in

160 We found that the catalytically inactive mutant of PI3Kgamma blocks the protection of PC

161 Furthermore, a catalytically inactive mutant of PKGIalpha bound RhoA but did not prev

162 An inactive mutant of PLZF abolishes this effect.

163 Expression of a catalytically inactive mutant of Pol eta increased replication fork st

164 Moreover, a catalytic inactive mutant of PP1alpha acted as dominant negative o

165 od cells, as compared with the catalytically inactive mutant of PTEN, which had no effect.

166 d by mutations of this site or when a kinase-inactive mutant of RSK was used.

167 However, a catalytically inactive mutant of SCP had no effect on Snail.

168 a number of promoters, whereas a phosphatase-inactive mutant of SCP1 enhances transcription.

169 Moreover, overexpression of a catalytically inactive mutant of SHP-2 inhibited p190-B RhoGAP tyrosyl

170 expression or overexpressing a catalytically inactive mutant of SHP-2.

171 e mutant of Gab1 (Gab1FF) or a catalytically inactive mutant of SHP2 (SHP2DN) prevented paxillin tyro

172 virus-mediated expression of a catalytically inactive mutant of SHP2 attenuated c-Src activation by b

173 se-2 (SHP2) augmented, whereas a phosphatase-inactive mutant of SHP2 inhibited, TNF-induced ASK1 deph

174 aining a stably expressed, but catalytically inactive mutant of Sir2p, sir2-345p, plus histone mutant

175 tumor cells more resistant, whereas a kinase-inactive mutant of SNARK sensitized cells to CD95-mediat

176 h SOD1(G85R) mice, which express a dismutase-inactive mutant of SOD1 and are considered a model of fa

177 The expression of a catalytically inactive mutant of TAK1 blocked XIAP/ILPIP synergistic a

178 DAC level was unaltered when the phosphatase-inactive mutant of TbTim50 was overexpressed, suggesting

179 s inhibited by expression of a catalytically inactive mutant of the class E VPS ATPase VPS4.

180 A catalytically inactive mutant of the enzyme is fused to the substrate

181 aminations is also seen with a catalytically inactive mutant of the enzyme showing that endonucleolyt

182 Overexpression of an inactive mutant of the regulatory alpha-subunit of PPTas

183 PK activity or expression of a catalytically inactive mutant of the upstream kinase MAPK kinase 3 (MK

184 d previously with a DNA-bound, catalytically inactive mutant of topoisomerase III where DNA binding r

185 cells with either the wild type or a kinase-inactive mutant of Tyk2 restores basal mitochondrial res

186 A catalytically inactive mutant of Ubp6 fails to recycle ubiquitin and a

187 o DNA was also studied using a catalytically inactive mutant of UNG and non-cleavable substrate analo

188 eVP40 VLP egress, and (iii) an enzymatically inactive mutant of WWP1 (C890A) did not ubiquitinate eVP

189 e molecular mechanism by which catalytically inactive mutants of CaMKIV exert their "dominant-negativ

190 splayed increased affinity for catalytically inactive mutants of Cdc14 compared with the wild-type ve

191 Two catalytically inactive mutants of CocE (S117A or Y44F) failed to prote

192 In this regard, the enzymatically inactive mutants of CT and LT, CTK63 and LTK63, and thei

193 The catalytically inactive mutants of Dlar were able to rescue Dlar(-/-) l

194 Four redox-inactive mutants of epimerase-active EryKR1 were enginee

195 Using catalytically inactive mutants of ERCC1-XPF and XPG, we show that the

196 sion of the kinase domain deleted and kinase-inactive mutants of hMINK beta in human fibrosarcoma HT1

197 onstructs of wild type hPLD1, mPLD2, and the inactive mutants of hPLD1 and mPLD2 resulted in associat

198 experiments with alkyl-transfer-active and -inactive mutants of human O(6)-alkylguanine DNA alkyltra

199 e rescued by wild type but not by the kinase-inactive mutants of IKK1 and IKK2, respectively.

200 TIRP also interacts with kinase-inactive mutants of IRAK and IRAK-4, IRAK-2, IRAK-M, and

201 Both wild-type and kinase-inactive mutants of IRAK and IRAK4, respectively, restor

202 ce to knock-in mice expressing catalytically inactive mutants of IRAK1 or IRAK4 prevented splenomegal

203 Rescue experiments with catalytically inactive mutants of MOF showed that its enzymatic activi

204 Overexpression of catalytically inactive mutants of phospholipase D (PLD) 1 or 2 attenua

205 Catalytically inactive mutants of PI5Kalpha had no effect on ENaC acti

206 Here we show that certain catalytically inactive mutants of PKK can activate NFkappaB, although

207 Conversely, overexpression of catalytically inactive mutants of PLD (hPLD1-K898R or mPLD2-K758R) or

208 al constructs of wild type and catalytically inactive mutants of PLD.

209 tallographic structures of two catalytically inactive mutants of protein-tyrosine phosphatase-like my

210 persisted for up to 120 min, whereas kinase-inactive mutants of S6K1 displayed only a reduced and tr

211 Kinase inactive mutants of TAK1 (TAK1DN) and PKR (PKRDN) inhibi

212 Coexpression of catalytically inactive mutants of the catalytic subunit of protein kin

213 was significantly higher than catalytically inactive mutants on Arabidopsis rin4/rps2 mutant plants,

214 wild-type (WT) and constitutively active or inactive mutants on endosomes were analyzed by fluoresce

215 P5KIgamma, but not by adding a catalytically inactive mutant or a splice variant lacking the talin-bi

216 AH-1 expressed in HEK 293T cells, but not an inactive mutant or inhibited enzyme.

217 ariants during treatment but not by protease inactive mutants or vector control.

218 Combined wild-type (WT) and inactive mutant P425R PCFTs were targeted to the cell su

219 ing in the expression of a transcriptionally inactive mutant p53 protein.

220 ctivation through the expression of a kinase inactive mutant, Pak1 K299R, or by treating tissues with

221 flies with similar overexpression of kinase-inactive mutant Par-1 or unphosphorylatable mutant Baz p

222 contrast, overexpression of a catalytically inactive mutant PCSK9 prevented the degradation of the m

223 ETS-1-dominant negative peptide (ETS-DN), an inactive mutant peptide (ETS-MU), or vehicle (n=6 per gr

224 tion in animals that received Met12, but not inactive mutant, peptide treatment.

225 c-specific overexpression of a catalytically inactive mutant PI3Kgamma, which disrupts the recruitmen

226 catalytic domain of PKA-alpha, catalytically inactive mutant PKA-alpha, or siRNA against PKA-alpha ca

227 erexpressed wild-type PLC-gamma1 or a lipase-inactive mutant PLC-gamma1 each augmented ACE in PC12 ce

228 e chemotactic response was, because a lipase-inactive mutant (PLD1-K830R) negated all chemokine-induc

229 tically inactive PLD1, but not catalytically inactive mutant PLD2 adenovirus, also increased Cch-stim

230 ta from chase experiments with catalytically inactive mutant Pol delta(AA).

231 g studies, demonstrates that the PDK1(S241A)-inactive mutant possesses an intact HM-pocket as well as

232 , wild-type EGLN3, but not its catalytically inactive mutant, potentiated myogenic differentiation.

233 ase by controlled mixing of wild type and an inactive mutant primase confirmed the oligomeric nature

234 of native PRL-1 as well as the catalytically inactive mutant PRL-1/C104S in complex with sulfate.

235 mixtures of R118A with inactive or virtually inactive mutants produced approximately 50% of the enzym

236 f wild-type CerS6, but not its catalytically inactive mutant, protected cells from cell death induced

237 site missense mutation leads to a mixture of inactive mutant protein (from translation with correctly

238 d via the X-ray structure of a catalytically inactive mutant protein bound to an A:oxoG-containing DN

239 Co-expression of active MBP-2C and inactive mutant proteins generated mixed oligomers that

240 esulted in association of PLD2 wild type and inactive mutant proteins with the PDGF-R beta compared w

241 se T activity from monomers derived from two inactive mutant proteins, one defective in catalysis and

242 ional disruption caused by the expression of inactive mutant PTEN protein.

243 teins containing wild-type and catalytically inactive mutant PTP1B was used to study the interaction

244 erexpression of PTP1B, but not catalytically inactive mutant PTP1B-C/S, inhibits VEGF-induced phospho

245 Expression of the constitutively GDP-bound, inactive mutant Rab11aS25N inhibits M4 trafficking to re

246 ECs, whereas overexpression of catalytically inactive mutant RAFTK/Pyk2 markedly suppressed HBMEC spr

247 expression of JMJD2A but not a catalytically inactive mutant reduced H3-K9/K36 trimethylation levels

248 erexpression of Jmj2 but not a catalytically inactive mutant reduced H3-Lys-4 trimethylation levels i

249 ression of a BRCC36 de-ubiquitinating enzyme-inactive mutant rescued both 53BP1 recruitment to DSBs a

250 Finally, Usp16, but not a catalytically inactive mutant, rescues the differentiation defects of

251 sion of wild-type hMMS21, but not its ligase-inactive mutant, rescues this hypersensitivity of hMMS21

252 knockdown or the overexpression of a kinase-inactive mutant resulted in enhanced cell proliferation

253 tituting one of the two active sites with an inactive mutant results in a significant reduction of th

254 he polymerase activity, in that a polymerase inactive mutant retained full 5'-dRP lyase activity.

255 ression of either USP20 or its catalytically inactive mutant revealed anti-inflammatory effects of US

256 transgenic mice overexpressing CAPN3 or its inactive mutant revealed that CaM binding enhanced CAPN3

257 11-1, proteasomes expressing a catalytically inactive mutant (rpn11(AXA)) were more stable and bound

258 By co-expression of wild type and inactive mutant S138C hRFCs, combined with surface bioti

259 nd A549 compared with expression of protease inactive mutants (S305A) or vector control.

260 e cofilin, an activated mutant (S3A), and an inactive mutant (S3E) demonstrated that altering cofilin

261 Exogenous expression of the catalytically inactive mutant Sac2C458S resulted in altered cellular d

262 animals expressing a SNARK dominant-negative inactive mutant (SDN) had increased myonuclear apoptosis

263 y, Trpc1(-/-) ECs or ECs transducing a TRPC1-inactive mutant showed a 1.5-fold increase in basal SPHK

264 cture with few adoptable conformations while inactive mutants showed a more flexible macrocycle which

265 Wild type (WT), but not catalytically inactive mutant SHP-2 (SHP-2 C459S), rescued the apoptot

266 f wild-type EGLN3, but not its catalytically inactive mutant, significantly inhibited NF-kappaB activ

267 Moreover, PIKE-A and its active and inactive mutants similarly enhance or antagonize U87MG c

268 se-active and approximately 90% of dismutase-inactive mutant SOD1 is bound to mitochondrial membranes

269 WASp association to PLD2-K758R, a lipase-inactive mutant, still occurs, albeit at lower levels, i

270 behavior for normal ATP turnover; and (iii) inactive mutant subunits inhibit the activity of spastin

271 s comprising distinctly tagged wild-type and inactive mutant subunits were purified at 1:1 stoichiome

272 eria against hydrogen peroxide), but not its inactive mutant suppressed aggregated protein formation

273 of wild-type PTPRF, but not the phosphatase-inactive mutant, suppressed cell proliferation and colon

274 rmore, expression of TET1 or a catalytically inactive mutant (TET1m) resulted in the upregulation of

275 s even more sensitive toward the presence of inactive mutants than in enzymatic assays, suggesting a

276 Bound iron was much lower in preparations of inactive mutants than in the wild-type protein.

277 thermore, we have identified a catalytically inactive mutant that does not respond to complex amino a

278 es of apo-PTP1B, the Michaelis complex of an inactive mutant, the phosphoenzyme intermediate, and the

279 s anemia virus Rev but not with functionally inactive mutants thereof.

280 Both the wild type Tpl2 and the kinase-inactive mutant Tpl2 K167M undergo Thr(290) phosphorylat

281 The inactive mutant transporters at position 351 could also

282 mase enzyme could be isolated from a pool of inactive mutants using a lacZ screen.

283 y reintroducing catalytically active but not inactive mutant USP15.

284 ubiquitylation, while either a catalytically inactive mutant USP8 or siRNA-mediated knockdown of USP8

285 ) cells with a noncleavable or catalytically inactive mutant version of caspase-1, we directly demons

286 We solved the structure of a catalytically inactive mutant version of Nsp15, which was crystallized

287 An inactive mutant (VKORC1(C132A/C135A)) was dominant negat

288 Overexpression of a catalytically inactive mutant Vps4 in Sulfolobus resulted in the accum

289 nd dark adapted forms and in photoactive and inactive mutants W104F and Q63L.

290 o that wild type ST3 but not a catalytically inactive mutant was sufficient to induce larval epitheli

291 hosphatase activity, because a catalytically inactive mutant was unable to protect cells from the eff

292 eurons expressing either dismutase active or inactive mutants was induction of neuronally derived com

293 tionally, through the expression of a kinase-inactive mutant, we have determined that Brk can mediate

294 Through the use of a kinase-inactive mutant, we show that MKK4 kinase activity is es

295 an initial purifying selection that removes inactive mutants; we identify approximately 100 variants

296 All inactive mutants were able to bind both substrates, ruli

297 of Mg(2+) on DNA binding, two catalytically-inactive mutants were constructed.

298 eIF4F bound the BTE and a translationally inactive mutant with high affinity, thus questioning the

299 identified were a number of photochromically inactive mutants with strong yellow or red fluorescence

300 f crystals of Y71F tyrosine phenol-lyase, an inactive mutant, with 3-F-l-Tyr with a dissociation cons