戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 or histocompatibility complex [MHC] class II invariant chain).
2 urface form of CD74 (MHC class II-associated invariant chain).
3 ues in the lumenal domain of human and mouse invariant chain.
4 La cells expressing only the p33 form of the invariant chain.
5 -A(b) mice deficient in both cathepsin L and invariant chain.
6 g peptide(s), in mice deficient for H2-M and invariant chain.
7 gous to that used by the class II-associated invariant chain.
8 DQ, and MHC class II-associated genes DM and invariant chain.
9 d by the fate of the class II chaperone, the invariant chain.
10 , CLIP, derived from the class II-associated invariant chain.
11 -associated invariant chain peptides) of the invariant chain.
12 his particular combination also precipitates invariant chain.
13  presentation through the degradation of the invariant chain.
14 expressed marginal levels of cathepsin S and invariant chain.
15 ins increased cell surface expression of the invariant chain.
16 association with the class II MHC chaperone, invariant chain.
17 diates processing of MHC class II-associated invariant chain.
18 into the modular pairwise association of CD3 invariant chains.
19  and related molecules, including the MHC II invariant chain (-2.73-fold).
20                                 LECs express invariant chain and cathepsin L, but not H2-M, suggestin
21 major contributor to the interaction between invariant chain and class II molecules.
22  of Nef to up-regulate the expression of the invariant chain and DC-SIGN at the cell surface, whereas
23 tant but contribute to the modulation of the invariant chain and DC-SIGN, and are least critical for
24 o not express the MHC II accessory molecules invariant chain and DM, they are likely to load addition
25 oncurrent proteolytic processing of both the invariant chain and endocytosed proteins.
26                              Coexpression of invariant chain and H-2M inhibit presentation of some, b
27 smic reticulum) are presented in the absence invariant chain and H-2M.
28 r CIITA and the CIITA targets, class II MHC, invariant chain and H2-DM (the murine equivalent of HLA-
29 cells by gamma-IFN induced the expression of invariant chain and HLA-DM alphabeta, thus facilitating
30 A-C, and the class II Ag presentation genes, invariant chain and HLA-DM, demonstrate that these prote
31 ecially cathepsins S and L, in degrading the invariant chain and regulating the convergence of proces
32 ult in the anomalous surface accumulation of invariant chain and the peptide-editing molecule H2-DM.
33 n S (Ctss), a cysteine protease that cleaves invariant chains and produces antigenic peptides for loa
34 scuss recent studies of the functions of TCR invariant chains and the contribution of the ten ITAMs t
35 antimature MHC class II antigen (lacking the invariant chain) and anti-CD20, both of which react with
36 lls transfected with genes for MHC class II, invariant chain, and DM, we have studied the contributio
37 r histocompatibility complex (MHC) class II, invariant chain, and DM.
38  (CLIP), a short proteolytic fragment of the invariant chain, and exhibit defective peptide-loading a
39 ents where the proper pH, proteases, MHC II, invariant chain, and HLA-DM reside, awaiting exogenous A
40  processing pathway, including class II MHC, invariant chain, and HLA-DMA/B genes.
41 ith promoters of immunoglobulin H chain, the invariant chain, and major histocompatibility complex cl
42 ification of an MHC-like compartment into an invariant chain- and MHC class II-rich complex of large
43 f CL or CS mediates efficient degradation of invariant chain as expected.
44                   MHC class II molecules and invariant chain assemble at a neutral pH in the endoplas
45 ow demonstrate that unlike newly synthesized invariant chain-associated MHC-II, mature cell surface p
46 compatibility complex (MHC) and the class II invariant chain-associated peptide (CLIP) occurs natural
47                                              Invariant-chain binding also directs class II molecules
48                                              Invariant chain binds to class II molecules and guides t
49 served sequence in an unstructured region of invariant chain, binds in the peptide binding groove of
50 HeLa cells expressing class II molecules and invariant chain by transfection.
51 ptide and is not free to interact with CLIP, invariant chain can still bind the class II molecule at
52 ences do not result in altered regulation of invariant chain catabolism.
53  activating expression of the p41 isoform of invariant chain CD74, which inhibits viral entry by bloc
54 ne protease essential for degradation of the invariant chain CD74.
55            Proteomic analysis identified the invariant chain (CD74) as a key substrate of Sppl2a and
56                                              Invariant chain (CD74) mediates antigen-presenting cell
57                                          The invariant chain (CD74) mediates assembly and targeting o
58                                          The invariant chain (CD74), a chaperone in MHC class II-medi
59  major histocompatibility complex-associated invariant chain (CD74), parvalbumin, and galectin-3-was
60 es (Hippocampus) featured a highly divergent invariant chain (CD74).
61  biogenesis, and the MHC-class-II-associated invariant chain chaperone has been reported to regulate
62  after cathepsin-mediated degradation of the invariant chain chaperone molecule.
63 rimarily associated with nested fragments of invariant chain (class II-associated invariant chain pep
64 ntity of the lysosomal enzyme that initiates invariant chain cleavage is dependent on the class II MH
65 lection defect is due solely to the block in invariant chain cleavage we analyzed cathepsin L-deficie
66 these defects are due solely to the block in invariant chain cleavage, we used cathepsin-deficient B
67  the MHC class II complex with a fragment of invariant chain (CLIP) during maturation.
68 cules in association with a peptide from the invariant chain (CLIP).
69 igens in association with a peptide from the invariant chain (CLIP).
70 as developed that allows the screening of an invariant chain-complementary DNA fusion library in a ge
71 l proteolytic degradation of alphabeta dimer-invariant chain complexes (alphabeta.I) within human B c
72 d in the endoplasmic reticulum with class II-invariant chain complexes and appears to be maintained t
73 wly synthesized cathepsin D and MHC class II-invariant chain complexes enter a non-clathrin-coated ve
74 I complex assembly, containing both class II-invariant chain complexes in the process of invariant ch
75 ly synthesized MHC class II and MHC class II-invariant chain complexes initially reside in a detergen
76 e intermediates in the transport of class-II-invariant chain complexes to antigen-processing compartm
77 light the taut interactions between class-II-invariant-chain complexes and endosomal proteases during
78                                  By using an invariant chain construct with various peptides engineer
79 n be greatly improved by the introduction of invariant chain constructs containing a T helper epitope
80 he major histocompatibility complex class II invariant chain cytoplasmic tail, indicating that the ef
81                                              Invariant chain deficiency in Ldlr(-/-) mice reduced ath
82 igen presentation by CD1d are not reduced by invariant chain deficiency.
83                                              Invariant chain-deficient (Ii -/-) mice have impaired ab
84 P also was abolished using APC obtained from invariant chain-deficient mice, demonstrating Ag present
85 epithelial cells use cathepsin L (Cat L) for invariant chain degradation and MHC class II maturation.
86 d that murine Cat S plays a critical role in invariant chain degradation in intestinal epithelial cel
87 homozygous mutant and wild-type animals, and invariant chain degradation was not impaired by deletion
88 to the cell surface, but was generated after invariant chain degradation within lysosomal-like MHC-II
89 ment of cells with leupeptin, which inhibits invariant chain degradation, leads to the accumulation o
90 pendent, and thus imply it is independent of invariant chain degradation.
91 s modified at its carboxyl terminus with the invariant chain-derived Ii-Key peptide and at its N term
92   Unlike long-lived A(b)/class II-associated invariant chain-derived peptide (CLIP) complexes, mature
93 xpress class II bound by class II-associated invariant chain-derived peptide (CLIP), a short proteoly
94  are loosely occupied by class II-associated invariant chain-derived peptide and are SDS unstable.
95 ng was modified in the presence of exogenous invariant chain-derived peptide suggests that both bindi
96 sion and decreases the relative level of the invariant chain-derived peptide, CLIP, bound to surface
97 lyzes the release of MHC class II-associated invariant chain-derived peptides (CLIP) from class II mo
98 gen processing by catalyzing the exchange of invariant chain-derived peptides (CLIP) from class II mo
99 isense oligonucleotides directed against the invariant chain enhances the presentation of mRNA-encode
100                                              Invariant chain expression is also greatly reduced, but
101                      Transient inhibition of invariant chain expression represents a simple and gener
102    This blockade resulted in the loss of the invariant chain fragment CLIP from the cell surface, sug
103 ng grooves were predominantly occupied by an invariant chain fragment or Ealpha(52-68) peptide, respe
104              HLA-DM catalyzes the release of invariant chain fragments from newly synthesized major h
105 partment(s) where antigenic peptides replace invariant chain fragments in the presence of the DM prot
106                            The generation of invariant chain-free MHC class II molecules and their as
107 n the endocytic pathway following removal of invariant chain from class II molecules and before their
108 proteolytic removal of the chaperone protein Invariant chain from MHC-II, degradation of internalized
109 ic immune enhancer (truncated shark class II invariant chain) fused to the nonstructural (NS) protein
110 man cancers, by screening a melanoma-derived invariant chain fusion cDNA library with tumor-reactive
111 tion sequence (TAT) and to part of the human invariant chain, generating a modular antigen transporte
112 ion of MHC class I, beta2-microglobulin, and invariant chain genes was also found in these RFX-B-defi
113 n up-regulated ICAM-1, VCAM-1, MHC class II, invariant chain, H2-M, CD40, and B7-1 as determined by F
114 g., LMP2), transporters of antigen peptides; invariant chain, HLA-DM, and the costimulatory molecule
115 ing signals in the context of HLA-DM and the invariant chain (I chain) complexed to HLA-DR.
116 n presentation, including il12, MHC class II invariant chain iclp1, and csf1r.
117         Class II proteins associate with the invariant chain (Ii chain) and its derived class II-asso
118 ation pathway, namely, the MHC-II-associated invariant chain (Ii or CD74) and the peptide editor H2-D
119 up-regulate class II transactivator (CIITA), invariant chain (Ii) (p31 and p41), H-2Ma, and H-2Mb.
120                                              Invariant chain (Ii) also associates with MHC class I mo
121          We have studied the consequences of invariant chain (Ii) and DM expression on major histocom
122 tant in class II-restricted Ag presentation, invariant chain (Ii) and DM.
123 the class II-associated accessory molecules, invariant chain (Ii) and DM.
124 nd related antigen processing genes, such as invariant chain (Ii) and H2-DM accessory molecules, are
125 ) is facilitated by the accessory molecules, invariant chain (Ii) and H2-M.
126 lass II pathways require both MHC-associated invariant chain (Ii) and HLA-DM (H2-M in mice) chaperone
127                The independent influences of invariant chain (Ii) and HLA-DM molecules on the array o
128 lass II molecules with peptides requires the invariant chain (Ii) and the class II-like molecule H-2M
129 ed complexes of MHC II alphabeta dimers with invariant chain (Ii) are targeted to endosomes, where Ii
130 yeast two-hybrid system was used to identify invariant chain (Ii) as a cellular protein that interact
131                             MHC class II and invariant chain (Ii) associate early in biosynthesis to
132                                              Invariant chain (Ii) associates with newly synthesized c
133 stocompatibility complex class II-associated invariant chain (Ii) binds to the active site of CatL an
134 proteases that not only destroy the class II invariant chain (Ii) chaperone but also generate the pep
135                                          The invariant chain (Ii) chaperone for MHC class II molecule
136 es, whereas biosynthetically immature MHC-II-Invariant chain (Ii) complexes are not.
137 patibility complex (MHC) class II-associated invariant chain (Ii) contains a 65 aa segment that binds
138  histocompatibility complex (MHC)-associated invariant chain (Ii) contains a single transmembrane dom
139 patibility complex (MHC) class II-associated invariant chain (Ii) contains an endoplasmic reticulum (
140 ine-based signals in the cytoplasmic tail of invariant chain (Ii) control targeting of newly synthesi
141 nd cathepsin L (catL) mediate late stages of invariant chain (Ii) degradation in discrete antigen-pre
142 invariant chain peptide (CLIP) region of the invariant chain (Ii) directly influences MHC class II pr
143 II major histocompatibility complex (Ia) and invariant chain (Ii) expression in the mouse intestinal
144 ired in this process both for degradation of invariant chain (Ii) from class II-Ii complexes to allow
145 ine-based motifs in the cytoplasmic tail and invariant chain (Ii) govern glycoprotein trafficking thr
146 nserted target Ag to MHC class II-associated invariant chain (Ii) greatly enhances both the presentat
147                             The MHC class II invariant chain (Ii) has been used as an adjuvant to enh
148 patibility complex (MHC) class II-associated invariant chain (Ii) has long been implicated in both co
149 oexpression of the MHC II accessory molecule invariant chain (Ii) inhibited presentation of endogenou
150                               Degradation of invariant chain (Ii) is a critical step in major histoco
151                                              Invariant chain (Ii) is a non-MHC-encoded molecule, whic
152 ted invariant chain peptide (CLIP) region of invariant chain (Ii) is believed to play a critical role
153                                         When invariant chain (Ii) is coexpressed with 81betaH-, the c
154 alent peptide (Ep), which in the presence of invariant chain (Ii) is extensively cleaved and replaced
155 lass II proteins and the class II-associated invariant chain (Ii) is important for proper MHC class I
156 T/E6 DNA with CIITA DNA and DNA encoding the invariant chain (Ii) linked to the pan HLA-DR-reactive e
157 ltering class II/CLIP affinity, we evaluated invariant chain (Ii) mutants with varying CLIP affinity
158                                          The invariant chain (Ii) plays a critical role in MHC class
159                                          The invariant chain (Ii) plays a critical role in the transp
160                   In I-A(b) mice lacking the invariant chain (Ii) processing enzyme, cathepsin S, NK1
161                                          The invariant chain (Ii) promoter was used as a model to det
162                   We studied the role of the invariant chain (Ii) protein's structure in its ability
163 patibility complex (MHC) class II-associated invariant chain (Ii) regulates intracellular trafficking
164                                          The invariant chain (Ii) targets major histocompatibility co
165                                          The invariant chain (Ii) targets newly synthesized major his
166 a glycosylation mutant of the p41 isoform of invariant chain (Ii) to evaluate the ability of ERAD to
167                      DP(84Gly) does not bind invariant chain (Ii) via the class II-associated invaria
168 y, APC expression of HLA-DRalphabeta and the invariant chain (Ii) was associated with faster internal
169 itively selected in Ab-Ep [Ab-Ep transgenic, invariant chain (Ii)(-/-), I-A beta(b-/-)] mice, where I
170 ng pathway and in the proteolytic removal of invariant chain (Ii), a critical regulator of MHC class
171 ecreased abundance of the p35 isoform of the invariant chain (Ii), a human-specific chaperone protein
172                                              Invariant chain (Ii), a third chain which is associated
173  antigenic peptides after degradation of the invariant chain (Ii), an MHC class II-associated protein
174 s II major histocompatibility complex (MHC), invariant chain (Ii), and cathepsin L (CatL) molecules i
175 tivator, which have defects in MHC class II, invariant chain (Ii), and H-2M (DM) expression, are resi
176 llular expression of the class II chaperone, invariant chain (Ii), during the late stages (i.e., 8-10
177  late stage processing of MHC class II-bound invariant chain (Ii), enabling dissociation of Ii, and b
178 decreases in IFN-gamma induced expression of invariant chain (Ii), H-2Ma, and H-2Mb mRNAs.
179 ells, its chaperone, the class II-associated invariant chain (Ii), is degraded in a stepwise fashion
180 ssion of the MHC class II accessory molecule invariant chain (Ii), or deletion of the MHC class II cy
181 re expressed by transfection without DRbeta, invariant chain (Ii), or DMbeta.
182 d numerous inflammatory genes, including MHC invariant chain (Ii), vascular cell adhesion molecule-1,
183  associate in the endoplasmic reticulum with invariant chain (Ii), which (i) mediates the delivery of
184 partments by the class II accessory molecule invariant chain (Ii), which itself must be eliminated to
185                                              Invariant chain (Ii)-deficient mice exhibit profound B c
186 -DM heterodimers mediate the dissociation of invariant chain (Ii)-derived class II-associated Ii pept
187 cells exposed to rapamycin that also express invariant chain (Ii)-FKBP in the ER.
188 ts is mediated by their association with the invariant chain (Ii).
189 ir interactions with the class II chaperone, invariant chain (Ii).
190 l front requires the MHC class II-associated invariant chain (Ii).
191 pendent on the groove binding section of the invariant chain (Ii).
192 ts is mediated by their association with the invariant chain (Ii).
193 and glycoprotein 100 (GP100) tethered to the invariant chain (Ii).
194 mmune defense, we focused our studies on the invariant chain (Ii).
195  study, we found the association of FcRn and invariant chain (Ii).
196 hey do not coexpress the class II-associated invariant chain (Ii).
197 ef protein upregulates the expression of the invariant chain (Ii)/major histocompatibility complex cl
198  histocompatibility complex (MHC)-associated invariant chain (Ii; CD74), which was found to be highly
199 ains, alpha and beta, which assemble with an invariant chain, Ii, in the endoplasmic reticulum.
200 stocompatibility antigen class II-associated invariant chain Iip35 exhibits dibasic retention, carrie
201 ed the proteolytic processing of CD74 MHC II invariant chain in both cell types, causing dramatic bui
202 ly of CD1d1 in vivo, akin to the function of invariant chain in MHC class II assembly.
203 ptides (derived from the class II-associated invariant chain) in exchange for more stably binding pep
204 omal processing pathway, cathepsin S and the invariant chain, in the normal functioning of CD1.
205 D1d may be altered by class II molecules and invariant chain induced during inflammation.
206 Moreover, MHC II and the class II-associated invariant chain influence CD1d trafficking.
207               There, the class II-associated invariant chain is degraded, and peptides derived from i
208 ransported to a low pH compartment where the invariant chain is trimmed to the class II-associated in
209    This binding between class II/peptide and invariant chain is weak, and coprecipitation is only app
210 4, the cell-surface form of the MHC class II invariant chain, is a key inflammatory factor that is in
211         CD74, or the class II MHC-associated invariant chain, is best known for the regulation of Ag
212 rface isoform of the MHC class II-associated invariant chain, is one such molecule; its role remains
213                             We show that the invariant chain (li, CD74) of the major histocompatabili
214 knockout DCs also accumulate high amounts of invariant chain-major histocompatibility complex (MHC) c
215      Accessory molecules, such as HLA-DM and invariant chain, modulate the ligands bound to MHC class
216            Cell-based vaccines consisting of invariant chain-negative tumor cells transfected with sy
217  the association with beta(2)-microglobulin, invariant chain of class II MHC, or patterns of glycosyl
218 and for the up-regulation of DC-SIGN and the invariant chain of MHC class II, but the role of the aci
219  was recently discovered and found to be the invariant chain of the HLA class II molecule, CD74.
220 sed activation motifs (ITAMs) present in the invariant chains of the TCR complex (TCR zeta and CD3-ga
221 ice show no differences in processing of the invariant chain or maturation of class II MHC products c
222 ulum (ER) via the N-terminal region of human invariant chain p33, with or without C-terminal KDEL, ma
223 derived from the cytoplasmic domain of human invariant chain (p33).
224 ted to a single peptide, class II-associated invariant chain peptide (CLIP) bound to H2-A(b).
225 ure of DQ2.5 is its high class-II-associated invariant chain peptide (CLIP) content.
226     Unlike the dominant role of one class II invariant chain peptide (CLIP) in blocking MHC class II,
227                      The class II-associated invariant chain peptide (CLIP) region of invariant chain
228                      The class II-associated invariant chain peptide (CLIP) region of the invariant c
229 ides engineered into the class II-associated invariant chain peptide (CLIP) region we have found that
230 riant chain (Ii) via the class II-associated invariant chain peptide (CLIP) region, nor does it prese
231 ragment of the Ii chain (class II-associated invariant chain peptide (CLIP) remains associated with c
232 etic exchange of the MHC class II-associated invariant chain peptide (CLIP) sequence with a sequence
233                          Class II-associated invariant chain peptide (CLIP), a conserved sequence in
234  mice have predominantly class II-associated invariant chain peptide (CLIP)-, not antigenic peptide-b
235  (MHC) by release of class II MHC-associated invariant chain peptide (CLIP).
236  chain is trimmed to the class II-associated invariant chain peptide (CLIP).
237 ollowing dissociation of class II-associated invariant chain peptide (CLIP).
238 ssociated with a loss of class II-associated invariant chain peptide and leupeptin-induced protein in
239 urthermore, the level of class II-associated invariant chain peptide bound to HLA-DQ did not correlat
240 ability, suggesting that class II-associated invariant chain peptide does not play a direct role in t
241 ng a T helper epitope by class II-associated invariant chain peptide exchange.
242 ression and cell surface class II-associated invariant chain peptide expression, which suggests that
243 with covalently tethered class II-associated invariant chain peptide or other peptides which bind rel
244 f tetramers from I-A(g7)/class II-associated invariant chain peptide precursors by peptide exchange.
245 y conserved and recognize a peptide from the invariant chain peptide presented by MHC class II.
246 talyzing the exchange of class II-associated invariant chain peptide with the antigen-derived peptide
247 he invariant chain termed CLIP (MHC class II invariant chain peptide) presented on MHC class II molec
248 -kD peptide termed CLIP (class II-associated invariant chain peptide).
249               DM removes class-II-associated invariant-chain peptide (CLIP) from newly synthesized cl
250  the half-life of HLA-DR1class II-associated invariant-chain peptide complexes.
251 n resulted in a shift of class II-associated invariant-chain peptide release curves by up to 0.5 pH u
252 atalyzes the exchange of class II-associated invariant chain peptides (CLIP) for antigenic peptides.
253 coexpressed with surface class II-associated invariant chain peptides (CLIP) in human EBV-positive an
254 that are occupied by MHC class II-associated invariant chain peptides (CLIP), indicating deficient lo
255 e loading and accumulate class II-associated invariant chain peptides (CLIP).
256 ecules is assisted by HLA-DM, which releases invariant chain peptides from newly synthesized MHCII an
257 ass II binding fragment (class II-associated invariant chain peptides) of the invariant chain.
258 ents of invariant chain (class II-associated invariant chain peptides), and their interaction with HL
259 e of peptides, including class II-associated invariant chain peptides, from MHC class II molecules.
260  most peptides, including classII-associated invariant chain peptides.
261  II MHC molecules and, by destruction of the invariant chain, prepares the class II MHC molecule for
262             Inhibition of AEP activity slows invariant chain processing and hinders the expression of
263        Furthermore, we observed no effect on invariant chain processing following AEP inhibition for
264 ) haplotype which has little dependence upon invariant chain processing for peptide presentation.
265                         Cathepsin L mediates invariant chain processing in cortical thymic epithelial
266 in B cells did not alter MHCII expression or invariant chain processing, but did perturb cytoplasmic
267                      However, the details of invariant-chain processing and antigen processing may di
268 G/Ii-CIITA, with the MHC class II-associated invariant chain promoter driving CIITA expression.
269  a modified form of GAD under control of the invariant chain promoter resulting in efficient epitope
270 complex (MHC) class II molecules without the invariant chain protein (Ii) that normally blocks the an
271 athrin trimerization domain with that of the invariant chain protein, were able to self-assemble in r
272 determined that cathepsin S is necessary for invariant chain proteolysis in T cells.
273 owed that assembly, endosomal transport, and invariant chain proteolysis of mutant DR3 molecules were
274 nhibition of endosomal proteases critical to invariant chain proteolysis reveals marked shunting of c
275 -invariant chain complexes in the process of invariant chain proteolytic removal as well as mature pe
276 te action of low pH and HLA-DM displaces the invariant chain remnant CLIP or other peptides from the
277 resentation by catalyzing dissociation of an invariant chain remnant from the peptide binding groove
278 eta- and gammadeltaTCRs also differ in their invariant chain subunit composition, in that alphabetaTC
279 ffector T cells recognize a peptide from the invariant chain termed CLIP (MHC class II invariant chai
280 ffector T cells recognize a peptide from the invariant chain termed CLIP in association with major hi
281 ly plays a regulatory role in processing the invariant chain that is associated with the major histoc
282 les bind to an accessory protein, termed the invariant chain, that ensures proper folding of the mole
283 cathepsin S (CS), have been shown to process invariant chain, thereby facilitating MHC class II matur
284 cines do not express the accessory molecule, Invariant chain, they present MHC II-restricted peptides
285 ng occurs after endosomal degradation of the invariant chain to a approximately 3-kD peptide termed C
286 a significantly impaired the ability of this invariant chain to accumulate stably at the immunologica
287 nic peptides but also for proteolysis of the invariant chain to allow the maturation of class II MHC
288 of major histocompatibility complex class II invariant chain to endosomal compartments.
289               We have studied the ability of invariant chain to interact with a class II molecule in
290  heterodimers that had to associate with the invariant chain to reach endosomal compartments.
291 nto complexes containing endogenous beta and invariant chains, transported to the trans-Golgi network
292 ity of CD1d trafficking and suggest that the invariant chain was a component of ancestral antigen pre
293                                          The invariant chain was further essential for endosomal tran
294 antigen presentation, namely cathepsin S and invariant chain, was determined.
295               Because the vaccine cells lack invariant chain, we have hypothesized that, unlike profe
296  an upregulation of surface HLA-DR and CD74 (invariant chain), whereas CLIP was slightly but signific
297 ains associate with a protein chaperone, the invariant chain, which promotes the proper assembly of M
298 plasma membrane and the endosome, and by the invariant chain, with which CD1d associates in the endop
299 d extensive acquisition of MHC-II, H-2M, and invariant chain within 30 min, with concurrent degradati
300 te processing of the MHC class II-associated invariant chain within B cells and dendritic cells, and

 
Page Top