ライフサイエンスコーパス: GALT

1 GALT catalyzes two consecutive reactions.

2 GALT CD8(+) T cells were predominantly CD45RO(+) and exp

3 GALT is also an important portal of entry for human immu

4 GALT protein abundance was increased in LA compared to D

5 GALT-DC-derived retinoic acid (RA) alone conferred gut t

6 Ep-tropic T cells follow a thymus-SI-Ep or a GALT-SI-Ep pathway, the latter generating highly competi

7 ree models: in SIVsmm-infected Rh, the acute GALT CD4+ T cell depletion was persistent and continued

8 ditional support that AtGALT2 encodes an AGP GALT was provided by two allelic AtGALT2 knock-out mutan

9 e of the identified metabolic genes, AGPAT6, GALT, GCLC, GSS, and RRM2B, were predicted to be dispens

10 MAdCAM-1 blockade reduced all GALT populations.

11 ssion of GALT cytokines (IL-4 and IL-10) and GALT specific adhesion molecules.

12 hat persistent HIV-1 in peripheral blood and GALT is found primarily in memory CD4(+) T cells [CD45RO

13 of CD4(+) T cells from peripheral blood and GALT was higher in patients who initiated treatment duri

14 but CD4(+)/CD8(+) T-cell ratios in blood and GALT were similar.

15 tween the odds ratios for ovarian cancer and GALT activity or the ratio of lactose intake to GALT act

16 PN reduces respiratory tract (RT) and GALT Peyer patch and lamina propria lymphocytes, lowers

17 s specific immunoglobulin A in the serum and GALT, taken on days 7, 14, and 21 postimmunization, clea

18 yte localization to the intestinal tract and GALT, and discuss their relevance to human intestinal ho

19 combinant human Gln188-, Arg188-, and Asn188-GALT and analyzed the first reaction in the absence of g

20 By contrast, both Arg188- and Asn188-GALT released more glu-1-P (170 +/- 8.0 and 129 +/- 28.4

21 T/min, whereas the mutant Arg188- and Asn188-GALT released only 600 +/- 71.2 and 2960 +/- 283.6 nmole

22 Over 300 disease-associated GALT mutations have been reported, with the majority bei

23 it NF-kappaB signaling and thereby attenuate GALT-promoting chemokine expression in the intestinal ep

24 ficant structural differences from bacterial GALT homologues in metal ligation and dimer interactions

25 Because GALT is a major portal of entry for HIV-1 and reservoir

26 ing the requirement for interactions between GALT and intestinal microflora in the selective expansio

27 )a B cells results from interactions between GALT and intestinal microflora.

28 nstrate a clear inverse relationship between GALT activity and galactose sensitivity.

29 nable model system of a relationship between GALT genotype, enzyme activity, sensitivity to galactose

30 odel to investigate the relationship between GALT, intestinal microflora, and modulation of the antib

31 scordance in CD4+ T-cell restoration between GALT and peripheral blood during therapy can be attribut

32 nance of normal CD4(+) T-cell levels in both GALT and peripheral blood.

33 The authors hypothesized that both GALT-depleting diets (intragastric and intravenous TPN)

34 dy showed that the retinoic acid produced by GALT dendritic cells (DCs) imprints B cells for gut homi

35 ee-dimensional model of the Escherichia coli GALT-UMP protein crystal.

36 ased activity of the LA variant, we compared GALT mRNA, protein abundance, and enzyme thermal stabili

37 mice that specifically lacked FDC-containing GALT only in the small intestine.

38 Although these mice had FDC-containing GALT throughout their large intestines, these tissues we

39 We have explored the possibility of covalent GALT heterogeneity using denaturing two-dimensional gel

40 entally, parenteral nutrition (PN) decreases GALT cell mass and mucosal immunity when compared with e

41 's patches from neonatal rabbits (designated GALT-less) and examined the extent to which VDJ genes we

42 ers of the commensal, intestinal flora drive GALT development through a specific subset of stress res

43 interact with intestinal microflora to drive GALT development and diversify the primary antibody repe

44 ive CD8(+) T cells are blocked from entering GALT.

45 We evaluated GALT enzyme activity and screened the GALT genes of 145

46 LTbetaR expression is critical for GALT control mechanisms and intact mucosal immunity.

47 The creation of a knockout mouse model for GALT deficiency was aimed at providing an organism in wh

48 To identify bacterial pathways required for GALT development, we introduced B. fragilis along with s

49 of the protein YqxM, which are required for GALT development.

50 displacement of glu-1-P with release of free GALT but impairs the subsequent binding of gal-1-P and d

51 We show that dendritic cells (DC) from GALT induce T cell-independent expression of IgA and gut

52 ucing plasma cells appear to be derived from GALT germinal centers in humans.

53 s indicated that AGP galactosyltransferases (GALTs) are members of the carbohydrate-active enzyme gly

54 Gln188-GALT displaced 80 +/- 7.0 nmol glu-1-P/mg GALT/min in th

55 Gln188-GALT produced 80,030 +/- 5,910 nmol glu-1-P/mg GALT/min,

56 Hence, GALT may function as a mammalian bursal homologue.

57 ic, did not promote GALT development; hence, GALT development in rabbits does not appear to be the re

58 applied a yeast expression system for human GALT to test the hypothesis that genotype will correlate

59 and that most T2 B cells isolated from human GALT are activated.

60 type of HIV-specific CD8(+) T cells in human GALT.

61 hough the microheterogeneity of native human GALT has long been recognized, the biochemical basis for

62 1.9 A resolution crystal structure of human GALT (hGALT) ternary complex, revealing a homodimer arra

63 In germinal center B cells of human GALT, Btk and Erk are phosphorylated, CD22 is down-regul

64 to elucidate activity of the wild-type human GALT enzyme.

65 ection was investigated using hyperimmunized GALT/KO mice as recipients of GAL+ heart allografts.

66 Immunized GALT/KO recipients of GAL+ heart transplants rejected th

67 rate that anti-GAL antibodies from immunized GALT/KO mice bind alphaGAL with an avidity/affinity simi

68 (G) along with a second, partially impaired GALT allele (Duarte-2, D2).

69 T activity and carry one profoundly impaired GALT allele (G) along with a second, partially impaired

70 t of innate immunity in B-cell activation in GALT compared with nonintestinal sites.

71 Activation in GALT is a previously unknown potential fate for immature

72 responses not only systemically but also in GALT.

73 ication in rabbit occurs well after birth in GALT, the diversification process may not be development

74 tetramers to assess HIV-specific T cells in GALT and reveal that GALT is the site of an active CD8(+

75 ls and IL-17 production from T(H)17 cells in GALT CD4(+) T cells.

76 Restoration of CD4+ T cells in GALT correlated with qualitative changes in SIV gag-spec

77 Both HIV- and CMV-specific CD8(+) T cells in GALT expressed CCR5, but only HIV-specific CD8(+) T cell

78 nd rapid reconstitution of CD4(+) T cells in GALT in animals receiving ART that were not observed in

79 Thus, activation of immature B cells in GALT may function as a checkpoint that protects against

80 tion and/or maintenance of CD4(+) T cells in GALT provides a more accurate assessment of the efficacy

81 population of resting memory CD4+ T cells in GALT to produce peak levels of virus that directly (thro

82 AART on the restoration of CD4(+) T cells in GALT.

83 ertoire and positive selection of B cells in GALT.

84 Germinal centers in GALT should be targets of mucosal vaccinations because t

85 As reported for humans, yeast deficient in GALT, but not their wild type counterparts, demonstrated

86 We show that CD4+ cell depletion in GALT correlates with the rapidity and greater magnitude

87 and propose a model in which they develop in GALT, self renew, continuously differentiate into mature

88 s direct evidence that B cell development in GALT may be driven by superantigen-like molecules, and f

89 BM, it is required for B cell development in GALT.

90 bbits, the primary Ab repertoire develops in GALT, and B cell expansion also occurs there.

91 Viral suppression was more effective in GALT of PHI patients than CHI patients during HAART.

92 stable proviral reservoir was established in GALT during primary HIV infection that persisted through

93 s a vitamin A metabolite highly expressed in GALT.

94 of T cell homeostasis and gene expression in GALT of three HIV-positive patients who initiated HAART

95 btilis promotes B cell follicle formation in GALT, and we investigated the mechanism by which B. subt

96 The role of restored CD4+ T-cell help in GALT during ART and its impact on antiviral CD8+ T-cell

97 ty controls the addressin balance of HEVs in GALT, the general HEV functionality is preserved indepen

98 L9)-specific CD8(+) T cells was increased in GALT relative to peripheral blood mononuclear cells by u

99 e initial host responses to HIV infection in GALT and the early molecular correlates of HIV enteropat

100 trate higher frequencies of HIV infection in GALT, compared with PBMCs, in these aviremic individuals

101 nnate activation of B cells were observed in GALT, compared with peripheral immune compartments.

102 gs indicate that HIV-induced pathogenesis in GALT emerges at both the molecular and cellular levels p

103 d birds, B cell lymphopoiesis takes place in GALT, such as the avian bursa of Fabricius.

104 CD4+ T-cell loss by 2 weeks postinfection in GALT but supported rapid and complete CD4+ T-cell restor

105 Surprisingly, T1 B cells were present in GALT, blood, and spleen of adult rabbits, long after B l

106 ls to diversify the primary Ab repertoire in GALT.

107 High levels of viral replication in GALT and marked CD4(+) T-cell depletion correlated with

108 complete suppression of viral replication in GALT during HAART correlated with increased HIV-specific

109 we provide evidence of viral replication in GALT resident CD4(+) T cells and macrophages in primary-

110 hment and persistence of viral reservoirs in GALT with minimal diversity.

111 Third, we found that the response in GALT was surprisingly low or undetectable, possibly cont

112 V-specific cell-mediated immune responses in GALT.

113 T cells in peripheral blood, restoration in GALT is delayed.

114 indicated that CD4(+) T-cell restoration in GALT was associated with up regulation of growth factors

115 ls had incomplete CD4+ T-cell restoration in GALT.

116 Loss of this regulation results in GALT hyperplasia and, in some animals, mucosa-associated

117 l priming may account for their retention in GALT.

118 nfection may perturb lymphocyte retention in GALT.

119 ukin (IL)-17 were increased significantly in GALT of DSS-treated mice.

120 h nodes, and inductive and effector sites in GALT.

121 ART led to viral suppression in GALT and peripheral blood mononuclear cells of PSI and C

122 Proviral variants in GALT and peripheral blood mononuclear cells (PBMCs) disp

123 e intestinal tropism of IgA ASCs elicited in GALTs but also the intestinal exclusion of lymphocytes p

124 ria triggers a protective immune response in GALTs and confers neuroprotection with improved locomoto

125 actor for ovarian cancer, although increased GALT activity attenuated the inverse association of oral

126 egregated with the LA phenotype of increased GALT activity in three different biochemical phenotypes

127 ia and that this nucleotide change increases GALT activity by increasing GALT protein abundance witho

128 change increases GALT activity by increasing GALT protein abundance without increasing transcription

129 We studied the mechanism of bacteria-induced GALT development.

130 Neither species alone consistently induced GALT development, nor did Clostridium subterminale, Esch

131 BBS prevents this TPN-induced GALT atrophy, depressed gastrointestinal and respiratory

132 Prion detection within large intestinal GALT biopsy specimens has been used to estimate human an

133 detection of prions within large intestinal GALT biopsy specimens has been used to estimate human an

134 tributions of the small and large intestinal GALT to oral prion pathogenesis were unknown.

135 We show that the small intestinal GALT are the essential early sites of prion accumulation

136 e data demonstrate that the small intestinal GALT are the major early sites of prion accumulation and

137 lly reduced in mice lacking small intestinal GALT.

138 in alpha4beta7 that effects their entry into GALT is downregulated following infection of mice with S

139 knock-out mutants, which demonstrated lower GALT activities and reductions in beta-Yariv-precipitate

140 Covariate-adjusted mean GALT activity was similar between cases (23.8 micro mol

141 lu-1-P (170 +/- 8.0 and 129 +/- 28.4 nmol/mg GALT/min, respectively).

142 88-GALT displaced 80 +/- 7.0 nmol glu-1-P/mg GALT/min in the first reaction.

143 +/- 71.2 and 2960 +/- 283.6 nmole glu-1-P/mg GALT/min, respectively.

144 LT produced 80,030 +/- 5,910 nmol glu-1-P/mg GALT/min, whereas the mutant Arg188- and Asn188-GALT rel

145 eir grafts within 2 hr although nonimmunized GALT/KO mice retained their grafts for up to 6 days.

146 mplex enteral diets and chow maintain normal GALT populations against established IgA-mediated antivi

147 deplete CD4+ T cells in the effector arm of GALT.

148 n commensal microbiota and lymphoid cells of GALT might affect the development of the peripheral B-ly

149 nt promotes formation of germinal centers of GALT, with no more evidence for innate immune receptor a

150 lecule MAdCAM-1, and other key components of GALT, all of which are important in increasing IgA level

151 However, the relative contributions of GALT in the small and large intestines to oral prion pat

152 individuals exhibited striking depletion of GALT CD4(+) T cells expressing CXCR4, CCR5, and alpha E

153 Massive acute depletion of GALT CD4+ T cells was a common feature of acute SIV infe

154 and reduces IgA levels through depression of GALT cytokines (IL-4 and IL-10) and GALT specific adhesi

155 Immunization of GALT/KO mice resulted in increased anti-GAL antibody exp

156 e background of C increased the incidence of GALT plasmacytomas by a factor of 2.5 in first-generatio

157 o SIV that are effective before infection of GALT.

158 od sample was collected to measure levels of GALT and to assay for the N314D (A940G) polymorphism of

159 ETOH feeding resulted in profound loss of GALT lymphoid cells and an increased number of Salmonell

160 The percentage of GALT CD8(+) T cells expressing alpha E beta 7 was signif

161 microbes and homed to the lamina propria of GALT.

162 bstantial plasticity in the specification of GALT HEV endothelium.

163 es of peripheral B cells from 2- to 5-mo-old GALT-less rabbits had undergone considerably less somati

164 s nasal-associated lymphoid tissue (NALT) or GALT, is thought to promote mucosal immunity.

165 crobial colonization and all other organized GALT was surgically removed.

166 hypothesis, we surgically removed organized GALT from newborn Alicia pups and ligated the appendix t

167 humans and galactosyltransferase knock-out (GALT/ KO) mice express high levels of anti-Gal antibodie

168 In both contexts, two predominant GALT species were observed.

169 Prenatal GALT development is dependent on ILC lymphoid-inducer fu

170 ric total parenteral nutrition (TPN) produce GALT atrophy, but only intragastric TPN preserves establ

171 ch by itself is immunogenic, did not promote GALT development; hence, GALT development in rabbits doe

172 members of the intestinal flora that promote GALT development.

173 and Bacillus subtilis consistently promoted GALT development and led to development of the preimmune

174 ce molecules of B. anthracis spores promoted GALT development.

175 In these remote colony rabbits, GALT was underdeveloped, and 70% of the Ig VDJ genes in

176 for lectin CD22 as a B-cell homing receptor GALT, and identification of the orphan G-protein-coupled

177 with Duarte galactosemia demonstrate reduced GALT activity and carry one profoundly impaired GALT all

178 otal parenteral nutrition (TPN) have reduced GALT T and B cells, the cells responsible for IgA produc

179 rnia, to examine the hypothesis that reduced GALT activity is associated with an increased risk of ov

180 Complete MAdCAM-1 blockade reduces GALT lymphocytes to PN levels, but the chow feeding stim

181 ta support a revised paradigm wherein severe GALT CD4+ T cell depletion during acute pathogenic HIV a

182 Surprisingly, GALT DCs, together with interleukin-5 (IL-5) and IL-6, a

183 HIV-specific T cells in GALT and reveal that GALT is the site of an active CD8(+) T-cell response dur

184 nce analysis of rebound virus suggested that GALT was not the major contributor to the postinterrupti

185 The GALT is therefore in the position of constantly fighting

186 her located APAH1 between the IL11RA and the GALT genes, thus excluding it as a candidate gene for ca

187 rs were maintained in both the blood and the GALT.

188 nce of viral reservoirs revolving around the GALT of HIV-infected individuals despite long-term viral

189 cating that TSE agent neuroinvasion from the GALT was impaired.

190 CD4+ T cells from the GALT, lymph nodes, and peripheral blood were isolated fr

191 CD8 T cells primed in the GALT acquired effector function and the capability to mi

192 We analyzed T-cell activation in the GALT and crossreactivity to the same antigen in the live

193 olangitis is caused by T cells primed in the GALT and provide the first link between colitis and chol

194 D11c(+) DCs were transiently depleted in the GALT and spleen before oral exposure, early agent accumu

195 re thought to initially differentiate in the GALT and/or mesenteric lymph nodes upon Ag encounter and

196 complete recoveries of CD4(+) T cells in the GALT of aviremic, HIV-infected individuals who had recei

197 degree and extent of HIV persistence in the GALT of infected individuals who had been receiving effe

198 icate that Tregs are rapidly depleted in the GALT of SIV-infected macaques, defining a role for the l

199 gulation of IL-4, IL-10, and TGF-beta in the GALT of wild-type but not microMT mice.

200 T cells, for which TLR costimulation in the GALT potently upregulates alpha4beta7 and enhances traff

201 ed in their ability to generate iTreg in the GALT when exposed to oral Ag, and 4-1BB-deficient mesent

202 ter infection with Trichuris, persist in the GALT, and mediate protective immunity to rechallenge.

203 ave shown that TSE agent accumulation in the GALT, in particular the Peyer's patches, is obligatory f

204 Inactivating mutations in the GALT-II gene (B3GALT6) associated with Ehlers-Danlos syn

205 the percentage of peripheral B cells in the GALT-less rabbits was generally less than that of contro

206 upon follicular dendritic cells (DCs) in the GALT.

207 ained depletion of CD4+ T lymphocytes in the GALT.

208 In treated animals that became infected, the GALT was significantly protected from infection and CD4(

209 Although T cells of the GALT are located in areas likely to have a key role in c

210 ay for the N314D (A940G) polymorphism of the GALT gene.

211 oy the follicle-associated epithelium of the GALT.

212 luated GALT enzyme activity and screened the GALT genes of 145 patients with one or more N314D-contai

213 -term viral suppression and suggest that the GALT may play a major role in the persistence of HIV in

214 Results showed that the GALT of naive wild-type and microMT mice was characteriz

215 the scrapie agent from the gut lumen to the GALT from which neuroinvasion subsequently occurs.

216 initially conveyed from the gut lumen to the GALT is not known.

217 When the GALT receives signals from the intestinal flora or food

218 pplement could be added to TPN to avoid this GALT atrophy and lower the incidence of infectious compl

219 Thus, GALT-DC shape mucosal immunity by modulating B cell migr

220 infections, gut-associated lymphatic tissue (GALT), the largest component of the lymphoid organ syste

221 phocytes in gut-associated lymphatic tissue (GALT).

222 roduction by gut-associated lymphoid tissue (GALT) after i.m. immunization.

223 primarily in gut-associated lymphoid tissue (GALT) after oral exposure to antigen and in a lymphopeni

224 y traffic to gut-associated lymphoid tissue (GALT) and have a key role in HIV and simian immunodefici

225 ent in human gut-associated lymphoid tissue (GALT) and involvement of innate immunity in B-cell activ

226 ion occur in gut-associated lymphoid tissue (GALT) and other lymphoid tissues (LT) since the early ph

227 onent of the gut-associated lymphoid tissue (GALT) and play an important role in mucosal immunity as

228 ls, homes to gut-associated lymphoid tissue (GALT) and that most T2 B cells isolated from human GALT

229 ode (LN) and gut-associated lymphoid tissue (GALT) biopsies from fully suppressed subjects, interrupt

230 rimed in the gut-associated lymphoid tissue (GALT) by a specific antigen migrate to the liver and cau

231 lue of acute gut-associated lymphoid tissue (GALT) CD4+ T cell depletion in lentiviral infections was

232 ha regulates gut-associated lymphoid tissue (GALT) formation in a noncell-autonomous manner.

233 al blood and gut-associated lymphoid tissue (GALT) from eight patients after 4-12 y of suppressive cA

234 Gut-associated lymphoid tissue (GALT) harbors the majority of T lymphocytes in the body

235 erruption on gut-associated lymphoid tissue (GALT) have not been well investigated.

236 cytes in the gut-associated lymphoid tissue (GALT) in the production of secretory IgA has been well c

237 Gut-associated lymphoid tissue (GALT) is a major site of HIV replication and CD4(+) T ce

238 Gut-associated lymphoid tissue (GALT) is a sensor region for luminal content and plays a

239 Gut-associated lymphoid tissue (GALT) is a significant but understudied lymphoid organ,

240 Gut-associated lymphoid tissue (GALT) is an early target for human immunodeficiency viru

241 Gut-associated lymphoid tissue (GALT) is an early target of human immunodeficiency virus

242 Although the gut-associated lymphoid tissue (GALT) is an important early site for human immunodeficie

243 The gut-associated lymphoid tissue (GALT) is constantly exposed to a variety of Ags and must

244 ) T cells in gut-associated lymphoid tissue (GALT) of animals infected with simian immunodeficiency v

245 usly" in the gut-associated lymphoid tissue (GALT) of interleukin-6 transgenic BALB/c (C) mice.

246 onent of the gut-associated lymphoid tissue (GALT) they may play a role in tolerance induction follow

247 e ability of gut-associated lymphoid tissue (GALT) to maintain mucosal immunity.

248 ofile in the gut-associated lymphoid tissue (GALT) was measured.

249 on occurs in gut-associated lymphoid tissue (GALT), and by about 1-2 mo of age nearly all Ig VDJ gene

250 cycle in the gut-associated lymphoid tissue (GALT), proliferated in the SI-Ep.

251 cells in the gut-associated lymphoid tissue (GALT), we first determine the distribution of Tregs in a

252 bacteria and gut-associated lymphoid tissue (GALT).

253 T cells from gut-associated lymphoid tissue (GALT).

254 , which is a gut-associated lymphoid tissue (GALT).

255 dentified in gut-associated lymphoid tissue (GALT).

256 home to the gut-associated lymphoid tissue (GALT).

257 cularly in gut-associated lymphatic tissues (GALT).

258 ases in the gut-associated lymphoid tissues (GALT) is important for efficient spread of disease to th

259 FDC) within gut-associated lymphoid tissues (GALT) is important for the efficient spread of disease t

260 ells in the gut-associated lymphoid tissues (GALT) were determined.

261 which lack gut-associated lymphoid tissues (GALT), such as Peyer's patches, and mature GP2(+) M cell

262 absence of gut-associated lymphoid tissues (GALT), such as Peyer's patches, which contain high numbe

263 elopment of gut-associated lymphoid tissues (GALT), which mediate a variety of host immune functions,

264 B cells in gut-associated lymphoid tissues (GALT).

265 he neonatal gut-associated lymphoid tissues (GALT).

266 lication in gut-associated lymphoid tissues (GALT).

267 ized gut-associated lymphoreticular tissues (GALT) and diffuse lamina propria, which give rise to muc

268 raining and gut-associated lymphoid tissues (GALTs) after systemic administration.

269 tivation in gut-associated lymphoid tissues (GALTs) and significant changes in the composition of bot

270 Gut-associated lymphoid tissues (GALTs) interact with intestinal microflora to drive GALT

271 and in the gut-associated lymphoid tissues (GALTs).

272 2, IL-17 or IL-13] and further contribute to GALT formation and function.

273 T activity or the ratio of lactose intake to GALT activity.

274 Although the homing of lymphocytes to GALT has been extensively studied, little is known about

275 of Ig genes in B cells that have migrated to GALT.

276 lage-hair hypoplasia, which maps proximal to GALT.

277 Mechanisms of T-cell recruitment to GALT and of T cells and plasmablasts to the small intest

278 B cells from peripheral lymphoid tissues to GALT may contribute to the generation of mucosal IgA res

279 arkers demonstrated that cell trafficking to GALT and not local proliferation contributed to CD4(+) T

280 omprises a significant fraction of the total GALT enzyme pool in normal human cells and that three of

281 educes hydrogen bonding and destabilizes UMP-GALT.

282 glutamine at position 188 stabilizes the UMP-GALT intermediate through hydrogen bonding and enables t

283 ose-1-phosphate (glu-1-P), and forms the UMP-GALT intermediate.

284 The unstable UMP-GALT allows single displacement of glu-1-P with release

285 man galactose-1-phosphate uridyltransferase (GALT) and is the most common mutation causing galactosem

286 the galactose-1-phosphate uridyltransferase (GALT) enzyme results in accumulation of galactose and it

287 of galactose-1-phosphate uridyltransferase (GALT) leads to significant neonatal morbidity and mortal

288 of galactose-1-phosphate uridyltransferase (GALT), which converts galactose-1-phosphate + UDP-glucos

289 Galactose-1-phosphate uridylyltransferase (GALT) acts by a double displacement mechanism, catalyzin

290 e galactose-1-phosphate uridylyltransferase (GALT) results in the potentially lethal disorder galacto

291 f galactose 1-phosphate uridylyltransferase (GALT).

292 f galactose-1-phosphate uridylyltransferase (GALT).

293 in other mammals, such as rabbits, that use GALT to develop and maintain the B cell compartment.

294 the postinterruption plasma viremia nor were GALT HIV reservoirs rapidly replaced by HIV rebound vari

295 To determine whether GALT is essential for somatic diversification, we surgic

296 However, whether GALT and/or mesenteric lymph nodes are required for inte

297 hypothesis that genotype will correlate with GALT activity measured in vitro and with metabolite leve

298 However, RA potently synergized with GALT-DC-derived interleukin-6 (IL-6) or IL-5 to induce I

299 hoid cells (ILCs) play a central role within GALT.

300 In young GALT/KO mice the levels of anti-GAL antibodies were low.