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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 presentation through the degradation of the invariant chain.
13 expressed marginal levels of cathepsin S and invariant chain.
14 his particular combination also precipitates 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.
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
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
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
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
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
49 served sequence in an unstructured region of invariant chain, binds in the peptide binding groove of
51 ptide and is not free to interact with CLIP, invariant chain can still bind the class II molecule at
57 major histocompatibility complex-associated invariant chain (CD74), parvalbumin, and galectin-3-was
58 biogenesis, and the MHC-class-II-associated invariant chain chaperone has been reported to regulate
60 rimarily associated with nested fragments of invariant chain (class II-associated invariant chain pep
61 ntity of the lysosomal enzyme that initiates invariant chain cleavage is dependent on the class II MH
62 lection defect is due solely to the block in invariant chain cleavage we analyzed cathepsin L-deficie
63 these defects are due solely to the block in invariant chain cleavage, we used cathepsin-deficient B
67 as developed that allows the screening of an invariant chain-complementary DNA fusion library in a ge
68 l proteolytic degradation of alphabeta dimer-invariant chain complexes (alphabeta.I) within human B c
69 d in the endoplasmic reticulum with class II-invariant chain complexes and appears to be maintained t
70 the trans-Golgi network (TGN), MHC class II-invariant chain complexes colocalized with the lysosomal
71 wly synthesized cathepsin D and MHC class II-invariant chain complexes enter a non-clathrin-coated ve
72 I complex assembly, containing both class II-invariant chain complexes in the process of invariant ch
73 ly synthesized MHC class II and MHC class II-invariant chain complexes initially reside in a detergen
74 e intermediates in the transport of class-II-invariant chain complexes to antigen-processing compartm
75 light the taut interactions between class-II-invariant-chain complexes and endosomal proteases during
77 n be greatly improved by the introduction of invariant chain constructs containing a T helper epitope
78 he major histocompatibility complex class II invariant chain cytoplasmic tail, indicating that the ef
82 P also was abolished using APC obtained from invariant chain-deficient mice, demonstrating Ag present
83 epithelial cells use cathepsin L (Cat L) for invariant chain degradation and MHC class II maturation.
84 d that murine Cat S plays a critical role in invariant chain degradation in intestinal epithelial cel
85 homozygous mutant and wild-type animals, and invariant chain degradation was not impaired by deletion
86 to the cell surface, but was generated after invariant chain degradation within lysosomal-like MHC-II
87 ment of cells with leupeptin, which inhibits invariant chain degradation, leads to the accumulation o
89 s modified at its carboxyl terminus with the invariant chain-derived Ii-Key peptide and at its N term
90 Unlike long-lived A(b)/class II-associated invariant chain-derived peptide (CLIP) complexes, mature
91 xpress class II bound by class II-associated invariant chain-derived peptide (CLIP), a short proteoly
92 are loosely occupied by class II-associated invariant chain-derived peptide and are SDS unstable.
93 ng was modified in the presence of exogenous invariant chain-derived peptide suggests that both bindi
94 sion and decreases the relative level of the invariant chain-derived peptide, CLIP, bound to surface
95 lyzes the release of MHC class II-associated invariant chain-derived peptides (CLIP) from class II mo
96 gen processing by catalyzing the exchange of invariant chain-derived peptides (CLIP) from class II mo
97 catalyzes the release of class II-associated invariant chain-derived peptides (CLIP) from newly synth
98 st notably, the level of class II-associated invariant chain-derived peptides (CLIP) is significantly
99 isense oligonucleotides directed against the invariant chain enhances the presentation of mRNA-encode
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
105 partment(s) where antigenic peptides replace invariant chain fragments in the presence of the DM prot
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 man cancers, by screening a melanoma-derived invariant chain fusion cDNA library with tumor-reactive
110 tion sequence (TAT) and to part of the human invariant chain, generating a modular antigen transporte
111 ion of MHC class I, beta2-microglobulin, and invariant chain genes was also found in these RFX-B-defi
112 n up-regulated ICAM-1, VCAM-1, MHC class II, invariant chain, H2-M, CD40, and B7-1 as determined by F
113 g., LMP2), transporters of antigen peptides; invariant chain, HLA-DM, and the costimulatory molecule
117 ation pathway, namely, the MHC-II-associated invariant chain (Ii or CD74) and the peptide editor H2-D
118 up-regulate class II transactivator (CIITA), invariant chain (Ii) (p31 and p41), H-2Ma, and H-2Mb.
123 nd related antigen processing genes, such as invariant chain (Ii) and H2-DM accessory molecules, are
125 lass II pathways require both MHC-associated invariant chain (Ii) and HLA-DM (H2-M in mice) chaperone
127 lass II molecules with peptides requires the invariant chain (Ii) and the class II-like molecule H-2M
128 ed complexes of MHC II alphabeta dimers with invariant chain (Ii) are targeted to endosomes, where Ii
129 yeast two-hybrid system was used to identify invariant chain (Ii) as a cellular protein that interact
132 stocompatibility complex class II-associated invariant chain (Ii) binds to the active site of CatL an
133 proteases that not only destroy the class II invariant chain (Ii) chaperone but also generate the pep
136 patibility complex (MHC) class II-associated invariant chain (Ii) contains a 65 aa segment that binds
137 histocompatibility complex (MHC)-associated invariant chain (Ii) contains a single transmembrane dom
138 patibility complex (MHC) class II-associated invariant chain (Ii) contains an endoplasmic reticulum (
139 ine-based signals in the cytoplasmic tail of invariant chain (Ii) control targeting of newly synthesi
140 nd cathepsin L (catL) mediate late stages of invariant chain (Ii) degradation in discrete antigen-pre
141 en shown in vitro to catalyze the release of invariant chain (Ii) derived peptides from the peptide-b
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
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
152 ted invariant chain peptide (CLIP) region of invariant chain (Ii) is believed to play a critical role
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
163 patibility complex (MHC) class II-associated invariant chain (Ii) regulates intracellular trafficking
166 a glycosylation mutant of the p41 isoform of invariant chain (Ii) to evaluate the ability of ERAD to
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
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
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
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
185 partments by the class II accessory molecule invariant chain (Ii), which itself must be eliminated to
187 -DM heterodimers mediate the dissociation of invariant chain (Ii)-derived class II-associated Ii pept
198 ef protein upregulates the expression of the invariant chain (Ii)/major histocompatibility complex cl
199 histocompatibility complex (MHC)-associated invariant chain (Ii; CD74), which was found to be highly
201 stocompatibility antigen class II-associated invariant chain Iip35 exhibits dibasic retention, carrie
202 ed the proteolytic processing of CD74 MHC II invariant chain in both cell types, causing dramatic bui
204 ptides (derived from the class II-associated invariant chain) in exchange for more stably binding pep
209 ransported to a low pH compartment where the invariant chain is trimmed to the class II-associated in
210 This binding between class II/peptide and invariant chain is weak, and coprecipitation is only app
211 4, the cell-surface form of the MHC class II invariant chain, is a key inflammatory factor that is in
213 rface isoform of the MHC class II-associated invariant chain, is one such molecule; its role remains
215 knockout DCs also accumulate high amounts of invariant chain-major histocompatibility complex (MHC) c
216 Accessory molecules, such as HLA-DM and invariant chain, modulate the ligands bound to MHC class
218 the association with beta(2)-microglobulin, invariant chain of class II MHC, or patterns of glycosyl
219 and for the up-regulation of DC-SIGN and the invariant chain of MHC class II, but the role of the aci
221 sed activation motifs (ITAMs) present in the invariant chains of the TCR complex (TCR zeta and CD3-ga
222 ice show no differences in processing of the invariant chain or maturation of class II MHC products c
223 ulum (ER) via the N-terminal region of human invariant chain p33, with or without C-terminal KDEL, ma
227 Unlike the dominant role of one class II invariant chain peptide (CLIP) in blocking MHC class II,
230 ides engineered into the class II-associated invariant chain peptide (CLIP) region we have found that
231 riant chain (Ii) via the class II-associated invariant chain peptide (CLIP) region, nor does it prese
232 ragment of the Ii chain (class II-associated invariant chain peptide (CLIP) remains associated with c
233 etic exchange of the MHC class II-associated invariant chain peptide (CLIP) sequence with a sequence
235 mice have predominantly class II-associated invariant chain peptide (CLIP)-, not antigenic peptide-b
239 ssociated with a loss of class II-associated invariant chain peptide and leupeptin-induced protein in
240 urthermore, the level of class II-associated invariant chain peptide bound to HLA-DQ did not correlat
241 ability, suggesting that class II-associated invariant chain peptide does not play a direct role in t
243 ression and cell surface class II-associated invariant chain peptide expression, which suggests that
244 with covalently tethered class II-associated invariant chain peptide or other peptides which bind rel
245 f tetramers from I-A(g7)/class II-associated invariant chain peptide precursors by peptide exchange.
247 talyzing the exchange of class II-associated invariant chain peptide with the antigen-derived peptide
248 he invariant chain termed CLIP (MHC class II invariant chain peptide) presented on MHC class II molec
252 n resulted in a shift of class II-associated invariant-chain peptide release curves by up to 0.5 pH u
253 atalyzes the exchange of class II-associated invariant chain peptides (CLIP) for antigenic peptides.
254 that are occupied by MHC class II-associated invariant chain peptides (CLIP), indicating deficient lo
256 ecules is assisted by HLA-DM, which releases invariant chain peptides from newly synthesized MHCII an
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.
261 II MHC molecules and, by destruction of the invariant chain, prepares the class II MHC molecule for
264 ) haplotype which has little dependence upon invariant chain processing for peptide presentation.
266 in B cells did not alter MHCII expression or invariant chain processing, but did perturb cytoplasmic
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
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
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
296 g biosynthesis, MHC class II associates with invariant chain which exists in two forms, p31 and p41.
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
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