ライフサイエンスコーパス: PIR

1 PIR also maintains NREF, a non-redundant reference datab

2 PIR can strongly influence the timing of spikes on rebou

3 PIR clones could form DNA-damage-induced RAD51 nuclear f

4 PIR maintains the Protein Sequence Database (PSD), an an

5 PIR technology enabled our team to precisely describe th

6 PIR-A and PIR-B are activating and inhibitory Ig-like re

7 PIR-A and PIR-B, paired immunoglobulin-like receptors en

8 PIR-ALN includes 529 alignments that can be used to deve

9 PIR-ALN is currently being distributed as a single ASCII

10 PIR-B coligation with the IgE receptor (FcepsilonRI) inh

11 PIR-B contains four ITIM motifs and is thought to be an

12 PIR-B negatively regulates macrophage functions in respo

13 PIR-B(-/-) BMMphi also produced more nitrite and TNF-alp

14 PIR-B(-/-) bone marrow-derived macrophages (BMMphi) fail

15 PIR-B(-/-) mice have more inflammatory cells in the live

16 PIR-B(-/-) mice were found to be more susceptible to Sal

17 PIR-B-deficient bone marrow eosinophils underwent compar

18 PIR-LAESI offers a 20-30 mum vertical resolution ( appro

19 PIR-LAESI was further used to image the distribution ins

20 PIR-LAESI was used to map the distribution of endogenous

21 PIR-NREF provides a timely and comprehensive collection

22 MBL proteins organized with more than 36 000 PIR superfamilies, 145 000 families, 4000 domains, 1300

23 In 2002, persons with ARED and a PIR of less than 1.50 were significantly less likely tha

24 In 1995 RESID was publicly released as a PIR-International text database distributed on CD-ROM an

25 late innate lung responses to P. murina in a PIR-B-independent manner.

26 significantly less likely than those with a PIR of at least 5 to report visiting an eye care provide

27 10.4 is shown to recognize an allelic PIR-A/PIR-B determinant on cells from BALB/c but not C57BL/6 m

28 ession could differentially affect the PIR-A/PIR-B equilibrium in different cell lineages.

29 e receptors (PIRs) that serve as activating (PIR-A) and inhibitory (PIR-B) receptors on B lymphocytes

30 Paired Ig-like receptors of activating (PIR-A) and inhibitory (PIR-B) isoforms are expressed by

31 the paired Ig-like receptors of activating (PIR-A) and inhibitory (PIR-B) types for modifying an IgE

32 rine paired Ig-like receptors of activating (PIR-A) and inhibitory (PIR-B) types, we isolated PIR hom

33 tibody 10.4 is shown to recognize an allelic PIR-A/PIR-B determinant on cells from BALB/c but not C57

34 Although PIR-B's inhibitory pathway has been described, it is unk

35 educational attainment (25.2; P = .049) and PIR (21.8; P = .01).

36 phages, two inhibitory receptors, SHPS-1 and PIR-B, are the major proteins binding to the tyrosine ph

37 PIR-A and PIR-B are activating and inhibitory Ig-like receptors on

38 ngs suggest that the disruption of PIR-A and PIR-B balance affects their regulatory roles in host def

39 determine the functional roles of PIR-A and PIR-B in primary bacterial infection, PIR-B-deficient (P

40 PIR allotype are expressed whereas PIR-A and PIR-B molecules bearing the maternal allotype are not.

41 elic expression of the polymorphic PIR-A and PIR-B molecules, and possibly of their human Ig-like tra

42 PIR-A and PIR-B, paired immunoglobulin-like receptors encoded, res

43 Although mast cells produced both PIR-A and PIR-B, PIR-B was found to be preferentially expressed on

44 ired immunoglobulin-like receptors PIR-A and PIR-B.

45 ctivating receptors referred to as PIR-B and PIR-A, respectively.

46 However, BIT and PIR-B are hypophosphorylated in motheaten macrophages, w

47 Finally, BIT and PIR-B associate with two tyrosyl phosphoproteins and a t

48 BIT and PIR-B bind preferentially to substrate-trapping mutants

49 Our data suggest that BIT and PIR-B recruit multiple signaling molecules to receptor c

50 1 dephosphorylates specific sites on BIT and PIR-B while protecting other sites from dephosphorylatio

51 membrane potential, endogenous bursting, and PIR properties could be observed in the intact nervous s

52 ession of 2 known ITAM antagonists, CD22 and PIR-B, was suppressed.

53 itory receptors (ILT3 and ILT4 in humans and PIR-B in rodents) and low levels of costimulatory and ad

54 ess with conjugate excitation-inhibition and PIR provides a reinforcing and evolutionarily advantageo

55 defined collectively by PROSITE patterns and PIR superfamilies.

56 omprehensive fragmentation of these PIRs and PIR-labeled cross-linked peptides with low-energy collis

57 ession of PIR-B, an inhibitory receptor, and PIR-A, an activating receptor; demonstrate the requireme

58 When combined, most BVM resistance and PIR mutations acted additively to impair viral replicati

59 f of the inhibitory receptors SIRP1alpha and PIR-B, which in turn recruit the phosphatase SHP-1.

60 onal information, the Swiss-Prot, TrEMBL and PIR protein database activities have united to form the

61 niProt Knowledgebase (Swiss-Prot, TrEMBL and PIR-PSD) using the standardized vocabulary of the Gene O

62 at NBRF.Georgetown.edu, directory [ANONYMOUS.PIR.ALIGNMENT].

63 erived macrophages, masking of PIR-B by anti-PIR mAb or genetic deletion of PIR-B shows significantly

64 The monoclonal anti-PIR antibody 10.4 is shown to recognize an allelic PIR-A

65 membrane glycoproteins, which we identify as PIR-B/p91A and the signal-regulatory protein (SIRP) fami

66 Inhibitory receptors such as PIR-B might be used as therapeutic targets for treatment

67 putative activating receptors referred to as PIR-B and PIR-A, respectively.

68 tation-tagged literature corpus developed at PIR was used to evaluate the system for finding phosphor

69 ch as paired immunoglobulin-like receptor B (PIR-B) and their function regulating eosinophil accumula

70 eptor paired immunoglobulin-like receptor B (PIR-B) in the regulation of macrophage function in innat

71 on of paired immunoglobulin-like receptor B (PIR-B), also known as leukocyte immunoglobulin-like rece

72 ficient in paired immunoglobulin receptor B (PIR-B), an inhibitory receptor activated by SFKs, did no

73 gh mast cells produced both PIR-A and PIR-B, PIR-B was found to be preferentially expressed on the ce

74 tatistically significant association between PIR and BMI z score among preterm boys (betaPIR + beta P

75 cells were much more likely to display both PIR and autapse-induced firing than GAD2(+) cells, suppo

76 The motif sequences are retrieved from both PIR-International and SWISS-PROT databases, including a

77 155 000 sequence entries retrieved from both PIR-International and SWISS-PROT databases.

78 Although mast cells produced both PIR-A and PIR-B, PIR-B was found to be preferentially ex

79 abase has been maintained collaboratively by PIR-International, an international association of data

80 ntries into families defined collectively by PIR superfamilies and PROSITE patterns.

81 ine signaling, whereas in hck-/-fgr-/- cells PIR-B was unphosphorylated.

82 Correspondingly, PIR-B was normally expressed on the cell surface of sple

83 zation (MALDI) were performed to corroborate PIR-LAESI images of the exogenous agent.

84 a non-redundant reference protein database, PIR-NREF.

85 rimary bacterial infection, PIR-B-deficient (PIR-B(-/-)) and wild-type (WT) control mice were injecte

86 We also demonstrate PIR-A3 interaction with the endogenous FcepsilonRIgamma

87 Rigorously designed PIR promotes global learning and local accountability.

88 mplitude or duration of IPSCs desynchronizes PIR activity in a population of TC cells.

89 e systematic detection of annotation errors, PIR has extended its superfamily concept and developed t

90 The expanded PIR WWW site allows sequence similarity and text searchi

91 Consistent with these findings, PIR-B negatively regulated eotaxin-dependent eosinophil

92 indicated that MDSCs genetically ablated for PIR-B (Lilrb3(-/-)) underwent a specific transition to M

93 earched expressed sequence tag databases for PIR relatives to identify chicken expressed sequence tag

94 veral in vitro studies, in vivo evidence for PIR remains scarce.

95 nsight supports a likely shared function for PIR-1 in C. elegans Furthermore, we show that DUSP11 mod

96 uence within this domain of IkappaBalpha for PIR degradation.

97 paBbeta, contained information necessary for PIR degradation, thereby explaining IkappaBalpha selecti

98 bservations point to a nonredundant role for PIR-B in the regulation of leukocyte integrin signaling.

99 suggest a physiological inhibitory role for PIR-B that is regulated by endogenous MHC class I-like l

100 sts of about 800 000 proteins collected from PIR-PSD, SWISS-PROT, TrEMBL, GenPept, RefSeq and PDB, wi

101 nsisting of more than 1 000 000 entries from PIR-PSD, SWISS-PROT, TrEMBL, RefSeq, GenPept, and PDB.

102 any multiple sequence alignment source (e.g. PIR and CLUSTAL formats), and is valuable for revealing

103 sprot, Swissnew, Trembl, Tremblnew, Genbank, PIR, Wormpep and PDB databases.

104 The criterion with the highest PIR was deemed the one with best performance.

105 The highest PIR was obtained with the progression criterion requirin

106 actor, the conserved RNA-phosphatase homolog PIR-1, is required for the processing of a putative ampl

107 Among girls, an increase in PIR was associated with a statistically significant decr

108 h greater national and global investments in PIR capacity will be required to enable the scaling of e

109 on: diffuse spreading along the sinusoids in PIR-B(-/-) mice vs nodular restricted localization in WT

110 The association between increased PIR and change in BMI z score varied by sex but not by r

111 -A and PIR-B in primary bacterial infection, PIR-B-deficient (PIR-B(-/-)) and wild-type (WT) control

112 urons were either presynaptically inhibited (PIR; 11%) or excited (PER; 8%) when extracellular glucos

113 eptors of activating (PIR-A) and inhibitory (PIR-B) isoforms are expressed by many hematopoietic cell

114 serve as activating (PIR-A) and inhibitory (PIR-B) receptors on B lymphocytes, dendritic cells, and

115 eptors of activating (PIR-A) and inhibitory (PIR-B) types for modifying an IgE antibody-mediated alle

116 eptors of activating (PIR-A) and inhibitory (PIR-B) types, we isolated PIR homologues from a rat sple

117 s, a protein family database that integrates PIR superfamilies and PROSITE motifs.

118 phosphorylated insulin receptor interacting (PIR) domain between the PH (pleckstrin homology) and SH2

119 85-kD molecules exclusively intracellularly; PIR-A and FcRgammac cotransfectants expressed the PIR-A/

120 PIRL ablation with electrospray ionization (PIR-LAESI) mass spectrometry is demonstrated and charact

121 A) and inhibitory (PIR-B) types, we isolated PIR homologues from a rat splenocyte cDNA library.

122 l surface molecules of approximately 120 kD, PIR-A transfectants expressed the approximately 85-kD mo

123 way, an RNA silencing role for the mammalian PIR-1 homolog (dual specificity phosphatase 11 [DUSP11])

124 The Ig-like receptor family member, PIR-B, has been shown to play an inhibitory role in rece

125 In Lyn-deficient mice, PIR-B tyrosine phosphorylation was greatly reduced.

126 beta(2)-microglobulin (beta(2)M) molecules, PIR-B served as a permissive checkpoint for IL-5-induced

127 proximately 25% amino acid identity to mouse PIR.

128 nsmembrane and cytoplasmic domains of murine PIR-A3 showed the ability of PIR-A3 to physically intera

129 The new PIR search systems have proved very useful in providing

130 s, our findings suggest that nonconventional PIR degradation of IkappaBalpha may play a physiological

131 BIT, but not PIR-B, is in a complex with the colony-stimulating facto

132 otation databases: Swiss-Prot, TrEMBL, NREF, PIR, Gene Ontology, KEGG, Entrez Gene, GenBank, GenPept,

133 mains of murine PIR-A3 showed the ability of PIR-A3 to physically interact with the FcepsilonRIgamma

134 y suppressing the proapoptotic activities of PIR-A, which were mediated by the Grb2-Erk-Bim pathway.

135 Surprisingly, the inhibitory activity of PIR-B was unimpaired in SHP-1-deficient mast cells.

136 phism data and search tools, the addition of PIR gene superfamily classifications, phenotype data for

137 Applications of PIR technology in host-pathogen interactions will enable

138 PIR-B by anti-PIR mAb or genetic deletion of PIR-B shows significantly impaired recognition of S. aur

139 ld account for the brain state dependence of PIR.

140 d not explain this brain state dependence of PIR.

141 In wild-type (wt) cells dephosphorylation of PIR-B was associated with maximal chemokine signaling, w

142 hese findings suggest that the disruption of PIR-A and PIR-B balance affects their regulatory roles i

143 in rats and mice, yet suggest divergence of PIR regulatory elements during rodent speciation.

144 e findings offer insights into the effect of PIR mutations on the evolution of BVM resistance in PI-e

145 crophage-rich region (MRR) at the expense of PIR DCs.

146 We also assessed expression of PIR-B human homologues (immunoglobulin-like transcript [

147 define the coordinate cellular expression of PIR-B, an inhibitory receptor, and PIR-A, an activating

148 However, the function of PIR-1 in RNAi has remained unclear.

149 The inhibitory function of PIR-B is mediated via its cytoplasmic immunoreceptor tyr

150 Cell surface levels of PIR molecules on myeloid and B lineage cells increased w

151 Eosinophils expressed high levels of PIR-B, and Pirb(-/-) mice displayed increased gastrointe

152 bone marrow-derived macrophages, masking of PIR-B by anti-PIR mAb or genetic deletion of PIR-B shows

153 Here, we examined the mechanisms of PIR degradation by comparing it to the canonical pathway

154 meric receptors to address the mechanisms of PIR-A signaling.

155 ved constitutive tyrosine phosphorylation of PIR-B molecules on macrophages and B lymphocytes, irresp

156 Unexpectedly, tyrosine phosphorylation of PIR-B was not observed in most myeloid and B cell lines

157 by maintaining the tonic phosphorylation of PIR-B.

158 Pearson) version of the annotated portion of PIR 39.

159 data are the first to show the potential of PIR-A3 to deliver activation signals to macrophages and

160 riments were performed to define the role of PIR-B in the negative regulation of macrophage function

161 To determine the functional roles of PIR-A and PIR-B in primary bacterial infection, PIR-B-de

162 Finally, the phosphorylation status of PIR-B was significantly reduced in MHC class I-deficient

163 Surprisingly, we found that the strength of PIR increased slowly over multiple cycles of synaptic in

164 matically alters the timing and synchrony of PIR.

165 on network and demonstrate the usefulness of PIR technology for precision mapping of functional host-

166 he inhibitory effect of increased glucose on PIR neurons appears to be mediated by a presynaptic gamm

167 s acquired most frequently with either WT or PIR PR.

168 n in the context of either wild-type (WT) or PIR PR, even at high BVM concentrations.

169 R amino acid sequences in a search for other PIR relatives led to the recognition of mammalian Fc rec

170 By analogy to the KIRs, p91/PIR-B may represent a novel class of macrophage receptor

171 e that pp130 is the product of the mouse p91/PIR-B gene that encodes a member of the killer cell inhi

172 ates that PIR molecules bearing the paternal PIR allotype are expressed whereas PIR-A and PIR-B molec

173 otein family databases (Blocks + DOMO, Pfam, PIR-ALN, PRINTS, PROSITE, ProDom, PROTOMAP, SBASE, and S

174 he monoallelic expression of the polymorphic PIR-A and PIR-B molecules, and possibly of their human I

175 The rat (ra) PIR-A and raPIR-B cDNA sequences predict transmembrane p

176 ment), and progression-to-improvement ratio (PIR) for each criterion.

177 ntire distributions of poverty-income ratio (PIR) and educational attainment.

178 sessed by using the poverty to income ratio (PIR), were associated with changes in BMI z score among

179 ool) and lower income (poverty income ratio [PIR] <1.00 vs >/= 4.00) were consistently less likely to

180 h as in the case of post-inhibitory rebound (PIR), and no neurons were found that displayed plateau p

181 verse inhibition and postinhibitory rebound (PIR) excitation of the pFRG and postinspiratory feedback

182 ng IPSCs accelerates postinhibitory rebound (PIR) in TC neurons, and that increasing either the ampli

183 Postinhibitory rebound (PIR) is believed to play an important role in the genesi

184 rease in the size of postinhibitory rebound (PIR) occurred with 5-HT application in all three cell ty

185 s 2 excitability and postinhibitory rebound (PIR), for the integrators that are typically used.

186 Many neurons exhibit postinhibitory rebound (PIR), in which neurons display enhanced excitability fol

187 their effect through the inhibitory receptor PIR-B since neutrophils and DCs from pir-b-/- mice were

188 we identify murine-paired Ig-like receptor (PIR)-B, and its human orthologs Ig-like transcript 2 and

189 ma)RIIB, gp49B1 and paired Ig-like receptor (PIR)-B, have shown that the molecules indeed suppress al

190 ated by paired immunoglobulin-like receptors PIR-A and PIR-B.

191 Paired immunoglobulin-like receptors (PIR) are expressed on B cells and macrophages and includ

192 Paired Ig-like receptors (PIR) that can reciprocally modulate cellular activation

193 urine equivalents, paired Ig-like receptors (PIR), contain two additional immunoglobulin domains, but

194 al antibodies produced against a recombinant PIR protein identified cell surface glycoproteins of app

195 consists of more than 200,000 non-redundant PIR and SWISS-PROT proteins organized with more than 28,

196 sion consists of about 830 000 non-redundant PIR-PSD, SWISS-PROT, and TrEMBL proteins organized with

197 The p21's PCNA interacting region (PIR), and not its CDK binding domain, is needed to preve

198 in the LN peripheral interfollicular region (PIR), DCs generate more frequent and stable interactions

199 rallel linear (SAM) and isotonic regression (PIR) methods identified 95 and 53 probe sets as dose-res

200 We used protein interaction reporter (PIR) technology to illustrate how viruses exploit host p

201 us [PLRV]) and protein interaction reporter (PIR), a revolutionary technology that couples a mass spe

202 nker was named protein interaction reporter (PIR).

203 s gap is policy and implementation research (PIR) that aims to produce generalizable evidence on what

204 We derived PARP-inhibitor-resistant (PIR) clones from the human CAPAN1 pancreatic cancer cell

205 , we observed that a PR inhibitor-resistant (PIR) HIV-1 mutant is unable to efficiently cleave the gp

206 luated the interplay between a PI-resistant (PIR) PR and the BVM resistance mutations in Gag.

207 ss-references, Protein Information Resource (PIR) and SWISS-PROT protein sequence database feature ta

208 The Protein Information Resource (PIR) has been maintaining a database of curated protein

209 The Protein Information Resource (PIR) has greatly expanded its Web site and developed a s

210 The Protein Information Resource (PIR) is an integrated public resource of protein informa

211 The Protein Information Resource (PIR) is an integrated public resource of protein informa

212 The Protein Information Resource (PIR) maintains a database of annotated and curated align

213 The Protein Information Resource (PIR) produces the largest, most comprehensive, annotated

214 The Protein Information Resource (PIR) serves as an integrated public resource of function

215 (SIB) and the Protein Information Resource (PIR).

216 (SIB) and the Protein Information Resource (PIR).

217 than proposed for Pre-Industrial Revolution (PIR) conditions has important ecological, biogeochemical

218 These results demonstrate that rhythmic PIR activity is an emergent property of interactions bet

219 ceptors which resemble the six domain rodent PIR as well as the four domain LILR found in other speci

220 Splenocyte PIR-B molecules were constitutively associated with the

221 We studied PIR in the lateral pyloric (LP) neuron of the stomatogas

222 d homodimer associated with the cell surface PIR molecules was identified as the Fc receptor common g

223 FcRgammac chain association for cell surface PIR-A expression; and suggest that the level of FcRgamma

224 a proteasome inhibitor-resistant, now termed PIR, pathway.

225 We conclude that PIR is cell type and brain state dependent and propose t

226 Moreover, we found that PIR degradation of IkappaBalpha and constitutive p50/c-R

227 cortical interneurons support the idea that PIR can serve as a network gamma mechanism.

228 This comparative study illustrates that PIR-LAESI is an ion source for ambient mass spectrometry

229 C57BL/6) F1 hybrid offspring indicates that PIR molecules bearing the paternal PIR allotype are expr

230 Here, we report that PIR can be observed in the dorsomedial entorhinal cortex

231 miniphosphoproteomic approach revealed that PIR-B recruits activating kinases after LTB(4) but not e

232 We further show that PIR-LAESI is capable of desorption ionization of protein

233 The PIR analysis was most sensitive for detecting transcript

234 The PIR databases and other files are also available by FTP

235 The PIR Protein Sequence Database entries are classified int

236 The PIR web site connects data analysis tools to underlying

237 The PIR web site features data mining and sequence analysis

238 The PIR web site features search engines that use sequence s

239 The PIR, in collaboration with the Munich Information Center

240 The PIR-Inter-national databases and search tools are access

241 The PIR-International databases and search tools are accessi

242 The PIR-International Protein Sequence Database and other fi

243 The PIR-International Protein Sequence Database and other fi

244 n expression could differentially affect the PIR-A/PIR-B equilibrium in different cell lineages.

245 off state, the HAMP is more compact, and the PIR samples a greater breadth of conformations.

246 e the amount of experimental annotation, the PIR has developed a bibliography system for literature s

247 f eye care services; SEP was measured by the PIR and educational attainment.

248 results in cleavage of the gp41 tail by the PIR PR.

249 t has been maintained collaboratively by the PIR-International, an association of data collection cen

250 al ensemble but correspondingly, compact the PIR.

251 sequence database in the public domain, the PIR-International Protein Sequence Database, in collabor

252 sequence database in the public domain, the PIR-International Protein Sequence Database.

253 tation was mapped to At5g18410, encoding the PIR/SRA1/KLK subunit of the ArabidopsisSCAR/WAVE complex

254 As expected, the PIR mutations had no effect on inhibition by BVM; howeve

255 es/macrophages, and mast cells expressed the PIR molecules in varying levels, but T cells and NK cell

256 and FcRgammac cotransfectants expressed the PIR-A/ FcRgammac complex on their cell surface.

257 explaining IkappaBalpha selectivity for the PIR pathway.

258 Sample questions for the PIR research agenda include how to close the gap in the

259 n also be obtained by anonymous FTP from the PIR FTP site at NBRF.Georgetown.edu, directory [ANONYMOU

260 cted with constructs having mutations in the PIR-B cytoplasmic region.

261 ons requiring standardized annotation in the PIR-International Protein Sequence Database was large an

262 nt interrelationships among sequences in the PIR-International Protein Sequence Database, to spread a

263 he standardized annotations appearing in the PIR-International Protein Sequence Database.

264 return with the inverted relationship in the PIR.

265 n and promote database interoperability, the PIR-International employs rule-based and classification-

266 olecular evidence for common ancestry of the PIR and Fc receptor gene families.

267 ing inverted repeats (PIR2), a member of the PIR family of fungal cell wall glycoproteins that protec

268 Stomata of an independent allele of the PIR gene (Atpir-1) showed reduced sensitivity to darknes

269 s. the pFRG and resultant modulations of the PIR in various excited and depressed states, leading to

270 ines but could be induced by ligation of the PIR molecules.

271 resistance was delayed in the context of the PIR PR, and the SP1-A1V mutation was acquired most frequ

272 hway to AME resistance in the context of the PIR PR, we selected for resistance with an HIV-1 isolate

273 e findings suggest that further study of the PIR-A receptors should be aggressively pursued toward a

274 Release 22.0, (December 1998), of the PIR-ALN database contains a total of 3806 alignments, in

275 ts define the preferential expression of the PIR-B molecules on mast cells and an inhibitory potentia

276 s, we investigated the effect of loss of the PIR-B protein on integrin-mediated signaling in primary

277 Inhibition of the PIR-B signaling pathway promoted MDSC differentiation in

278 bases and search tools are accessible on the PIR web site at http://pir.georgetown.edu/ and at the MI

279 In 1998 it was made available on the PIR Web site at http://www-nbrf.georgetown.edu/pir/searc

280 bases and search tools are accessible on the PIR WWW site at http://pir.georgetown.edu and at the MIP

281 n Information Database (JIPID), produces the PIR-International Protein Sequence Database (PSD), the m

282 l system can be used to browse and query the PIR-ALN alignments.

283 l system can be used to browse and query the PIR-ALN alignments.

284 dependent RNA polymerase (RdRP) requires the PIR-1 phosphatase.

285 New capabilities for searching the PIR sequence databases include annotation-sorted search,

286 he database is freely accessible through the PIR Web site http://pir.georgetown.edu/pirwww/dbinfo/res

287 led scores perform slightly better; when the PIR database is used, Altschul-Gish scaled scores perfor

288 cation in Jurkat T cells associated with the PIR mutations, even in the absence of compound.

289 formationally destabilized compared with the PIR, whereas in the kinase-off state, the HAMP is more c

290 eraction is dependent on Arg(632) within the PIR-A3 transmembrane domain.

291 ped on the basis of their expression of this PIR allelic determinant.

292 o the major protein (PDB, SWISS-PROT/TrEMBL, PIR-ALN, NCBI Taxonomy Browser) and literature (PubMed,

293 d in PROSITE and mostly detected from unique PIR sequences.

294 Whereas PIR-B fibroblast transfectants expressed cell surface mo

295 paternal PIR allotype are expressed whereas PIR-A and PIR-B molecules bearing the maternal allotype

296 f splenocytes from FcRgammac-/- mice whereas PIR-A was not.

297 or tyrosine-based inhibitory motifs, whereas PIR-A pairs with the Fc receptor common gamma chain to f

298 ay has been described, it is unknown whether PIR-A receptors can deliver activation signals to macrop

299 ines of evidence supporting a model in which PIR-B displays opposing but potent regulatory functions

300 l education (trend P = .036), and those with PIR 1.00-1.99 (trend P < .001).