ライフサイエンスコーパス: type III

1 of the N-terminal 3(10)-helix and beta-turn type III.

2 tion defects by early overexpression of NRG1 type III.

3 better understanding of the organization of Type III-A CRISPR effector complexes as well as highligh

4 tal structures of Staphylococcus epidermidis Type III-A CRISPR subunits Csm2 and Csm3 and a 5.2 angst

5 Csm6 therefore provides robustness to the type III-A CRISPR-Cas immune response against difficult

6 rRNA maturation and establish a link between Type III-A CRISPR-Cas immunity and central nucleic acid

7 Csm, a type III-A CRISPR-Cas interference complex, is a CRISPR

8 Target RNA binding to crRNA-bound type III-A CRISPR-Cas multi-subunit Csm surveillance com

9 Type III-A CRISPR-Cas surveillance complexes containing

10 Type III-A CRISPR-Cas systems are prokaryotic RNA-guided

11 Type III-A CRISPR-Cas systems employ the Cas10-Csm compl

12 lp to clarify the quaternary architecture of Type III-A effector complexes, and provide details on cr

13 f the in vitro and in vivo activities of the type III-A M. tuberculosis CRISPR system.

14 icroscopy to study the interaction between a type III-A ribonucleoprotein complex and various RNA sub

15 When mutations in the fibronectin type III and kinase domains of EPHB1 were compared with

16 ananatis lacks both the virulence-associated type III and type II secretion systems.

17 Markers of interstitial matrix type III and V collagen formation (PRO-C3 and PRO-C5), b

18 understanding of the natural history of SMA type III and will be helpful in the interpretation of th

19 xpression of procollagen type I, procollagen type III, and alpha-smooth muscle actin, areas of pronou

20 , acquired angioedema, hereditary angioedema type III, and angiotensin converting enzyme inhibitor-in

21 patients with spinal muscular atrophy (SMA) type III assessed using the Hammersmith Functional Motor

22 teins and in vitro assays, we define how the type III-B effector from the hyperthermophilic bacterium

23 e RNase and DNase activities associated with Type III-B immunity in Pyrococcus furiosus (Pfu) are reg

24 ndings define the target requirement for the type III-B system from T. maritima and provide a framewo

25 otic activity, and osteotomy site healing in type III bone and high endogenous Wnt signaling.

26 virus infection induces robust production of type III, but not type I, interferon (IFN).

27 A GBS type III capsular polysaccharide (CPS)-tetanus toxoid co

28 Type III cells (aka "synaptic cells") are elongate with

29 About one-quarter of Type III cells also exhibit an atypical mitochondrion ne

30 ency significantly reduced the expression of type III cells compared with that in wild type (WT) mice

31 daas; finally, OY phytoplasmas entered into type III cells of salivary glands at 21-28 daas.

32 anterior midgut of the alimentary canal and type III cells of salivary glands were identified as the

33 layed a tooth phenotype resembling human DGI type III characterized by enlarged dental pulp chambers,

34 opment, establish an in vivo function of CHD Type III chromatin remodeling proteins in this process,

35 SMV was recovered from H type III-coated beads for 13 stool specimens out of 27 S

36 coated beads, the mean percent recovery by H type III-coated beads was 308.11% +/- 861.61.

37 Collagen type III (COL3) is one of the 3 major collagens in the b

38 otease (MMP)-degraded type I collagen (C1M), type III collagen (C3M), type IV collagen (C4M) and a pr

39 eoepitope-specific N-terminal pro-peptide of type III collagen (Pro-C3) than placebo.

40 type IV collagen (C4M) and a pro-peptide of type III collagen (PRO-C3) were measured by ELISA in pre

41 neoepitope-specific N-terminal propeptide of type III collagen (Pro-C3; -22% and -33%) and enhanced l

42 ous connective tissue composed of type I and type III collagen fibers.

43 degradation (C3M) and formation (PRO-C3) of type III collagen further, higher PRO-C3 was associated

44 ormation was enhanced by 19%, and the type I/type III collagen ratio was shifted toward higher abunda

45 showed that FKBP22 catalyzed the folding of type III collagen through its prolyl isomerase activity

46 nsile strength, and a higher ratio of type I:type III collagen.

47 ivity and acted as a molecular chaperone for type III collagen.

48 , geometric mean concentrations of serum GBS type III CPS-specific immunoglobulin G were 12.6 ug/mL (

49 molecule, allowing viruses to neutralize the type III CRISPR defence system.

50 enylate second messenger produced during the type III CRISPR immune response.

51 ), and demonstrated that viruses can subvert type III CRISPR immunity by means of a potent anti-CRISP

52 d Rossman fold (CARF) subunits co-opted from type III CRISPR immunity.

53 he complex regulatory mechanisms controlling Type III CRISPR immunity.

54 rthermore, we show for the first time that a type III CRISPR system can be reprogrammed by replacing

55 Type III CRISPR systems are unique, as their targeting m

56 ologues of this enzyme (named Crn2) exist in type III CRISPR systems but are uncharacterised.

57 Type III CRISPR systems detect foreign RNA and activate

58 Type III CRISPR systems detect viral RNA, resulting in t

59 On binding invading RNA species, Type III CRISPR systems generate cyclic oligoadenylate (

60 (cOA) secondary messengers are generated by type III CRISPR systems in response to viral infection.

61 Type III CRISPR systems synthesise cyclic oligoadenylate

62 Type III CRISPR systems synthesise cyclic oligoadenylate

63 In type III CRISPR systems, an effector complex programmed

64 Type III CRISPR-Cas prokaryotic immune systems provide a

65 Cas10 is the signature gene for type III CRISPR-Cas surveillance complexes.

66 ffector complex is similar to those found in type III CRISPR-Cas systems and that this feature is spe

67 Type III CRISPR-Cas systems employ guide RNA to recogniz

68 Upon target RNA recognition, type III CRISPR-Cas systems produce cyclic-oligoadenylat

69 Type III CRISPR-Cas systems provide immunity to foreign

70 e CARFs are components of a CBASS built into type III CRISPR-Cas systems, where the CARF domain binds

71 ystems, we identify NucC homologs in over 30 type III CRISPR/Cas systems, where they likely function

72 Upon target RNA interaction, Type III crRNP effector complexes become activated to cl

73 ) cells by conferring mutations in Dicer1, a type III cytoplasmic endoribonuclease involved in small

74 emonstrated that the Sulfolobus solfataricus type III-D CRISPR complex generates cyclic tetra-adenyla

75 he X-ray structure of a truncated monomer of Type III Dio (Dio3), which deiodinates TH inner rings th

76 ke homolog 1 (Dlk1)-deiodinase iodothyronine type III (Dio3) locus are up-regulated in an mTORC1-depe

77 cellular leucine rich repeat and fibronectin Type III domain containing 1) is necessary to generate f

78 Fibronectin type III domain containing 5 (Fndc5) is a transmembrane

79 Irisin is a product of fibronectin type III domain-containing protein (Fndc5) and is involv

80 membrane-bound precursor protein fibronectin type III domain-containing protein 5 (FNDC5), also expre

81 ynonymous variants affecting the fibronectin type III domain.

82 en the membrane-proximal (third) Fibronectin type III domains (Fn3) of Tie2.

83 smembrane proteins with multiple fibronectin type III domains following the N-terminal Sema domain (t

84 were analyzed in additional type I/II versus type III EBV latency DLBCL cell lines.

85 During EBV infection, type III EBV latency genes were expressed rapidly after

86 Upon transcript binding, DNA cleavage by type III effector complexes is activated.

87 e, Wu et al. (2019) propose that a bacterial type III effector modifies the host milieu specifically

88 nt species and targeted by several bacterial type III effector proteins including the cysteine protea

89 The candidate type III effector TarP, which localized to focal adhesio

90 tivator-like effectors (TALEs) are bacterial Type-III effector proteins from phytopathogenic Xanthomo

91 e involved in adherence and translocation of type III effectors into the host cells.

92 Most plant bacterial pathogens rely on type III effectors to cause diseases.

93 21 or TCF21) and mature (periostin, collagen type III) fibroblast gene signatures.

94 C2 type (IgC2) domains and four fibronectin type III (FnIII) domains that are shared with many other

95 AS that selectively binds to two fibronectin type III (FnIII) repeats within cellular fibronectin, sp

96 d-optimal temperatures, predators may have a type III functional response, and prey carrying capacity

97 l electronic instability, and display broken type-III gap, thus offering optimal carrier density with

98 sentative of the protective response against type III GBS polysaccharide.

99 ative of the protective response against the type III group B Streptococcus polysaccharide was compri

100 In this study, we engineered a class of type III hammerhead ribozymes to develop RNA switches th

101 ains (Prugniaud/type II/haplogroup 2 and CEP/type III/haplogroup 3) and monitored mouse weight, survi

102 Neuregulin-1 Type III has been proposed to activate calcineurin signa

103 Hereditary sensory and autonomic neuropathy type III (HSAN III) is a rare neurological condition tha

104 hereditary sensory and autonomic neuropathy type III (HSAN III), also known as Riley-Day syndrome or

105 provide a comprehensive review of type I and type III IFN activities, highlighting shared and distinc

106 and especially the less adverse effect-prone type III IFN are good candidates for the management of C

107 Thus, our model system identified type I or type III IFN as potential antiviral treatments for COVID

108 IFN-lambda4 is a unique type III IFN because it is produced only in individuals

109 with that in wild-type mice, indicating that type III IFN exacerbates lung inflammation.

110 ly dependent on MDA5/MAVS signaling, whereas type III IFN expression was entirely dependent on MDA5/M

111 infection these mice had increased levels of type III IFN expression, neutralization of which reduced

112 l cells (IECs) are particularly dependent on type III IFN for the control and clearance of virus infe

113 , the preferential responsiveness of IECs to type III IFN in vivo enables selective ISG expression du

114 Type III IFN lambdas (IFN-lambda) have recently been des

115 nfected mice with a knockout mutation in the type III IFN receptor (IFNLR1) and double IFNAR1/IFNLR1

116 s in ISG expression that mirrors the in vivo type III IFN response.

117 lence factor that suppresses both type I and type III IFN responses.IMPORTANCE Coronaviruses (CoVs) c

118 In vitro treatment of IEC organoids with type III IFN results in ISG expression that mirrors the

119 standing of ligand-receptor interactions for type III IFN signaling and highlight the importance of t

120 Here, we confirm that type III IFN treatment elicits robust and uniform ISG ex

121 ress in our understanding of both type I and type III IFN-mediated innate antiviral responses against

122 increased in magnitude and scope relative to type III IFN.

123 ' cGAMP or dsDNA, pDC-s produced type I, and type III IFN.

124 iviral interferons of type I (IFN-alpha) and type III (IFN-lambda) against SARS-CoV-2 and compared th

125 ssion of type I (IFN-alpha and IFN-beta) and type III (IFN-lambda1 to IFNlambda3) IFNs than viruses e

126 IFN lambda (type III-IFN-lambda1) is a molecule primarily produced b

127 including the role of the mucosa-restricted type III IFNs (IFN-III), informing our understanding of

128 scientific community working in the field of type III IFNs (IFN-lambda) realized that this class of I

129 interferons (IFNs) (IFN-alpha, IFN-beta) and type III IFNs (IFN-lambda) share many properties, includ

130 signaling cascades, but unlike type I IFNs, type III IFNs (IFNlambda) do not elicit strong inflammat

131 hoblasts through the constitutive release of type III IFNs (IFNlambda1 and IFNlambda2) and become res

132 Type I IFNs act systemically, whereas type III IFNs act preferentially at epithelial barriers.

133 ls (pDCs) are potent producers of type I and type III IFNs and play a major role in antiviral immunit

134 s into the immunobiology of SLE and identify type III IFNs as important factors for tissue-specific p

135 a signaling cascade that induces type I and type III IFNs as well as other cytokines, to generate an

136 Although type I and type III IFNs can activate STAT1 and STAT2, triple-negat

137 fer a spatiotemporal division of labor where type III IFNs control viral spread at the site of the in

138 report in Science that type III IFNs disrupt epithelial cell proliferation and

139 Type III IFNs failed to induce IRF1 expression because o

140 n understanding of the biology of type I and type III IFNs in health and disease.

141 IFN-lambda4 acted faster than other type III IFNs in inducing antiviral genes, as well as ne

142 We discuss a model wherein type III IFNs serve as a front-line defense that control

143 Type III IFNs, or IFN-lambda, are the newest members of

144 ust transcriptional activation of type I and type III IFNs.

145 uman and mouse cell lines through type I and type III IFNs.

146 ribonucleases, Csx1 or Csm6, can promote the Type III immune response by destroying both invader and

147 This and the fact that Type III immunity can be provided by plasmid-borne mini-

148 ipts survived the infection, indicating that Type III immunity does not operate through altruistic su

149 Phages that escaped Type III interference accumulated deletions of integral

150 through a second messenger generated by the type III interference complex.

151 G(2)/M arrest strongly inhibited type I and type III interferon (IFN) production as well as expressi

152 ovirus (RV) by mounting antiviral type I and type III interferon (IFN) responses.

153 cultures with the immune molecules type I or type III interferon (IFN) was able to inhibit SARS-CoV-2

154 Type III interferon (IFN), or IFN lambda (IFN-lambda), i

155 We identified a predominant type III interferon (IFN)-mediated innate response to Hu

156 Type III interferon (IFN-lambda) is important for innate

157 Using a genetic approach to disrupt murine type III interferon cytokine genes Ifnl2 and Ifnl3, we f

158 port the idea of an exclusive role for known type III interferon cytokines in signaling via IFNLR to

159 ng mice lacking the Ifnlr1 gene encoding the type III interferon receptor have demonstrated that sign

160 both the type I interferon response and the type III interferon response in macrophages and epitheli

161 of key bile acid receptors that regulate the type III interferon response.

162 tly in vitro but induced stronger type I and type III interferon responses.

163 L-10R family and highlight the plasticity of type III interferon signaling and its therapeutic potent

164 controlling the production of IFNlambda4, a type III interferon.

165 e proximal gut involves bile acid priming of type III interferon.

166 In this study, we assessed how type III interferons (IFN-lambda) contribute to the path

167 NiV infection resulted in the expression of type III interferons (IFN-lambda).

168 Type I and type III interferons (IFNs) activate similar antiviral t

169 es to this ongoing global threat, type I and type III interferons (IFNs) are currently being evaluate

170 This in turn stimulates production of type III interferons and hence enhances tumour antigen p

171 lation of mucosal viral pathogens.IMPORTANCE Type III interferons are potent antiviral cytokines impo

172 These findings emphasize the importance of type III interferons in regulation of a variety of viral

173 factors that induce synthesis of type I and type III interferons(1).

174 1D produce Abs directed against the neuronal type III intermediate filament protein peripherin.

175 equired by type I IRES but not by type II or type III IRES, in which cleavage of eIF4GI has not been

176 very of selective CSF1R inhibitors devoid of type III kinase activity has proven to be challenging.

177 pe I IFN and type II IFN (IFN-gamma), but no type III (lambda) IFN has been identified.

178 e transcripts are regulated similarly to EBV type III latency genes and that TET2 protein is a cofact

179 cofactor of EBNA2 and coregulator of the EBV type III latency program and DNA methylation state.IMPOR

180 Here we ask if modulating NRG1 type III levels in neurons would restore myelination in

181 Recovery by H type III ligands was subject-specific and weakly correla

182 ce from the canonical "autoreceptor" role of Type III mGluRs, and substantially altering synaptic pha

183 ood samples for 25(OH)VD and the procollagen type III N-terminal peptide (P3NP) were collected at bas

184 Third, interaction of 3 to 5 drivers (type III; n=42) with changing areas of control.

185 n-Type III-nitride nanowires decorated with Ru sub-nanoclu

186 Axonal neuregulin 1 type III (Nrg1TIII) drives peripheral nerve myelination

187 itor binding mode has proven challenging and Type III or Type IV allosteric inhibitors may present a

188 Hereditary sensory and autonomic neuropathy type III, or familial dysautonomia [FD; Online Mendelian

189 ) PADI3 encodes peptidyl arginine deiminase, type III (PADI3), an enzyme that post-translationally mo

190 n addition, we found that mice infected with type III parasites, which are supposed to be less virule

191 evelopment and defence by its involvement in type III peroxidase-mediated polymer cross-linking, lign

192 mbrane NADPH oxidases, peroxisomal oxidases, type III peroxidases and other apoplastic oxidases.

193 eptor cells (TRCs) expressing otopetrin 1 on type III presynaptic TRCs on the tongue, which were prev

194 The chromatin modifier PRMT7 is the only Type III PRMT found in higher eukaryotes and a restricte

195 PRMT7 is the single type III PRMT solely capable of arginine monomethylation

196 Type III protein secretion systems are essential virulen

197 Type III protein secretion systems have specifically evo

198 Type III protein-secretion machines are essential for th

199 Endoglin (Eng), a type III receptor for the TGF-beta superfamily, has been

200 in Arabidopsis thaliana reveal a role of the type III receptor PYRABACTIN RESISTANCE-LIKE 2 for the a

201 from the axonal protein neuregulin 1 (NRG1) type III regulate Schwann cell fate and myelination.

202 i) metal coordination to the organic ligand (type III), respectively.

203 Analysis of phase-variable Type I and Type III restriction-modification systems in multiple hu

204 th phase variation switching the activity of Type III RMS, and both the activity and specificity of a

205 ative genomic analysis demonstrated that the type III secreted effector EspT gene, an autotransporter

206 lasmids in dissemination of a unique E. coli type III secreted effector that is involved in host inva

207 iting phosphoprotein (Tarp) is a multidomain type III secreted effector used by Chlamydia trachomatis

208 Type III secreted effectors (T3SEs) can be injected into

209 e predictor developed to accurately identify type III secreted effectors from protein sequence data.

210 e virulence factors in xanthomonads, such as type III secreted effectors including transcription acti

211 While other type III secreted effectors of E. coli have been identif

212 ExoU, a type III secreted phospholipase effector of Pseudomonas

213 ted by the injectisome in a process known as type III secretion (T3S).

214 anipulates host cells by injecting them with type III secretion effector proteins.

215 ndent transcriptional regulator hilA and the type III secretion effector sopB >200- and 68-fold, resp

216 types associated with different steps in the type III secretion process.

217 smic conduit that provides a pathway for the type III secretion substrates to reach the entrance of t

218 inflammasome upon sensing components of the type III secretion system (T3SS) and flagellar apparatus

219 plant cell wall degrading enzymes (PCWDEs), type III secretion system (T3SS) and flagellar motility.

220 the enteropathogenic Escherichia coli (EPEC) type III secretion system (T3SS) effector translocated i

221 We examined the importance of type III secretion system (T3SS) effectors in the produc

222 The type III secretion system (T3SS) is a pivotal virulence

223 an opportunistic pathogenic bacterium whose type III secretion system (T3SS) plays a critical role i

224 cal inflammasome activation by the conserved type III secretion system (T3SS) rod proteins from Gram-

225 Here, we show that AxoU is a type III secretion system (T3SS) substrate that induces

226 ny pathogenic Gram-negative bacteria use the type III secretion system (T3SS) to deliver effector pro

227 Pseudomonas aeruginosa uses a type III secretion system (T3SS) to inject cytotoxic eff

228 Many Gram-negative pathogens use a type III secretion system (T3SS) to promote disease by i

229 um Salmonella pathogenicity island 1 (SPI-1) type III secretion system (T3SS)) and outer membrane (OM

230 arahaemolyticus, can be exported through the type III secretion system (T3SS), which engages in one-s

231 isplayed greatly increased expression of the Type III secretion system (T3SS), widely considered to b

232 howed that during colonic crypt hyperplasia, type III secretion system (T3SS)-mediated intimate epith

233 the Salmonella pathogenicity island 1 (SPI1) type III secretion system (T3SS).

234 entery, plague, and typhoid fever, rely on a type III secretion system - a multi-membrane spanning sy

235 solic Salmonella via the invasion-associated Type III Secretion System 1 (T3SS1).

236 t and eggs, and virulence in humans requires type III secretion system 1 (TTSS-1), encoded on Salmone

237 Concomitantly, endosymbiont genes encoding a type III secretion system and a flagellum apparatus are

238 he epithem and is actively suppressed by the type III secretion system and its effector proteins.

239 interior (apoplast), while genes involved in type III secretion system and syringomycin synthesis wer

240 The Pseudomonas aeruginosa type III secretion system delivers effector proteins dir

241 ExoU is a potent type III secretion system effector that, after secretion

242 We previously identified a bacterial type III secretion system effector, termed NleD, a metal

243 C. rodentium injects type III secretion system effectors into intestinal epit

244 re of the export apparatus of the Salmonella type III secretion system in association with the needle

245 This process is promoted by type III secretion system inactivation in infected tissu

246 cies deliver Yop effector proteins through a type III secretion system into host cells.

247 ctive capacity of Yersinia YopB, a conserved type III secretion system protein, alone or combined wit

248 re of the T4aP secretin from the type II and type III secretion system secretins.

249 filament protein of a Salmonella Typhimurium type III secretion system that are involved in the regul

250 P. aeruginosa uses its type III secretion system to secrete various effector pr

251 ive agent of plague, Yersinia pestis, uses a type III secretion system to selectively destroy immune

252 crV, the needle cap protein of the Y. pestis type III secretion system, binds to the N-formylpeptide

253 enes encoding a molecular syringe known as a type III secretion system, leading to infectious colitis

254 epithelium invasion is promoted by O(2) in a type III secretion system-dependent manner.

255 required for extracellular survival and the type III secretion system-the symbiont's primary virulen

256 um of which the main virulence factor is the Type III Secretion System.

257 he Salmonella pathogenicity island 1 (SPI-1) type III secretion system.

258 eutrophils from destruction by the Y. pestis type III secretion system.

259 ets identified the mRNA for the regulator of type III secretion system.

260 needle protein PrgI from the S. Typhimurium type III secretion system.

261 Many Gram-negative bacterial pathogens use type III secretion systems (T3SS) to inject proteins int

262 ogens interact with mammalian cells by using type III secretion systems (T3SS) to inject virulence pr

263 ted substrates also called effectors through Type III secretion systems (T3SSs) into host cells and c

264 Bacterial type III secretion systems (T3SSs) play an important rol

265 Many Gram-negative bacteria use type III secretion systems (T3SSs) to inject virulence e

266 can be injected into host cell cytoplasm via type III secretion systems (T3SSs) to modulate interacti

267 Aurodox downregulates the expression of the type III secretion systems of enteropathogenic and enter

268 tion systems work by cryoEM, with a focus on type III secretion systems.

269 insights into how the ATPase contributes to type III secretion, including torque generation and bind

270 men of its central channel in the control of type III secretion.

271 This mode of protein export is termed type-III secretion (T3S).

272 EHEC) engages a syringe-like machinery named type-III secretion system (T3SS) to inject effectors wit

273 te that the modulation of axon-to-glial NRG1 type III signaling has beneficial effects and improves m

274 We studied Type III spacer acquisition in phage-infected Thermus th

275 Here, we demonstrate that a model type III system in Staphylococcus epidermidis relies upo

276 e show that Csx3 is strongly associated with type III systems and that Csx3 binds cyclic tetra-adenyl

277 Type III systems are found in diverse archaea and bacter

278 for understanding the target requirements of type III systems as a whole.

279 Unlike type I and type II systems, type III systems do not require a protospacer adjacent m

280 While some Type III systems encode a reverse transcriptase to acqui

281 Type III systems exhibit a robust immune response that c

282 Type III systems must differentiate between invader and

283 Taken together, these results suggest that Type III systems primarily target transcripts, instead o

284 al hybrid with similarity to both type I and type III systems.

285 e PFS is recognized may vary among different type III systems.

286 h the fungus Rhizopus microsporus, bacterial type III (T3) secretion is known to be essential.

287 tributes to sour taste sensing by regulating type III taste cell differentiation in mice.

288 Acids are detected by type III taste receptor cells (TRCs), located in taste b

289 viability and expression of collagen type I, type III, tenomodulin, and phosphorylated AKT.

290 The type III TGF-beta receptor (TbetaRIII) is a TGF-beta co-

291 Gene induction is mediated by a type III transcription activator-like effector.

292 -selective ion channel Otop1 is expressed in type III TRCs and is a candidate sour receptor.

293 is required for the inward proton current in type III TRCs from different parts of the tongue that ar

294 We next show that in type III TRCs from Otop1-KO mice, intracellular pH does

295 t trains of action potentials, as they do in type III TRCs from wild-type mice.

296 Axonal factors, such as Neuregulin-1 Type III, trigger promyelinating signals that upregulate

297 Usher syndrome type III (USH3) characterized by progressive loss of vis

298 tirely visible; type II: vallecula obscured; type III: vallecula and glottis obscured), as well as ob

299 terminated AF and required more ablation in types III versus I (P=0.02 in left atrium).

300 ons of FKBP22, which preferentially binds to type III, VI and X collagens, but not to type I, II or V