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1 s in the tumor suppressor genes pRB, p53 and KAI1.
2  D11S1344, which is located in the region of KAI1.
3 argely blocked by concomitant suppression of KAI1.
4 nown as gp-Fy), as an interacting partner of KAI1.
5                       The product of CD82 is KAI1, a 40- to 75-kDa tetraspanin cell-surface protein a
6                Suppression of gp78 increases KAI1 abundance and reduces the metastatic potential of t
7 ets the transmembrane metastasis suppressor, KAI1 (also known as CD82), for degradation.
8 ial cells through direct interaction between KAI1 and DARC, and that this interaction leads to inhibi
9 dies of the tumor metastasis suppressor gene KAI1 and plasminogen activator inhibitor 1 (PAI1), defin
10       Comparisons of gene structures between KAI1 and seven other members of the transmembrane 4 supe
11  of the percentage of cells that stained for KAI1 and the intensity of the stain (1, 2, or 3).
12  KDELR3 regulates the metastasis suppressor, KAI1, and report an interaction with the E3 ubiquitin-pr
13 ns of TGF-beta receptors, E-cadherin, C-CAM, KAI1, and some integrins have an inverse correlation wit
14 ts indicate that the cancer cells expressing KAI1 attach to vascular endothelial cells through direct
15                                    NDRG1 and KAI1 belong to metastasis suppressor genes, which impede
16  of not only the tumor metastatic suppressor KAI1 but also of hepatic cytochromes P450, is upregulate
17       The transmembrane 4 superfamily member KAI1 (CD82) has been shown to inhibit pulmonary metastas
18 ovement, but not for the association between KAI1/CD82 and alpha3beta1 integrin.
19  events critical for motility are altered by KAI1/CD82 and how KAI1/CD82 regulates these events.
20 on regulates the subcellular distribution of KAI1/CD82 and its association with other tetraspanins, s
21 l-surface protein physically associated with KAI1/CD82 and named it KASP: a KAI1/CD82-associated surf
22 s are needed for proper interactions between KAI1/CD82 and tetraspanins CD9 and CD151, which also reg
23                       Distinctive from known KAI1/CD82 associations that usually occur in the context
24                 Cancer metastasis suppressor KAI1/CD82 belongs to the tetraspanin superfamily and inv
25 AI1/CD82, overexpression of p130CAS in Du145-KAI1/CD82 cells increased the formation of p130CAS-CrkII
26 witch" in cell motility, was formed in Du145-KAI1/CD82 cells.
27 nd Lyn, however, remained unchanged in Du145-KAI1/CD82 cells.
28   In transmembrane (TM) domains, tetraspanin KAI1/CD82 contains an Asn, a Gln, and a Glu polar residu
29 erent tetraspanins, and its association with KAI1/CD82 could be independent of CD81 and CD9.
30 ctin reorganization; at the molecular level, KAI1/CD82 deregulated Rac1, RhoA, and their effectors co
31  for the functional integrity of tetraspanin KAI1/CD82 during the suppression of cancer cell migratio
32                                         Upon KAI1/CD82 expression, Rac effector cofilin was not enric
33 of the plasma membrane became deficient upon KAI1/CD82 expression.
34 egulated at both RNA and protein levels upon KAI1/CD82 expression.
35 tions of microprotrusion and microvesicle to KAI1/CD82 function.
36            Furthermore, EWI2/PGRL synergizes KAI1/CD82 in inhibiting cell migration, indicating that
37            In summary, at the cellular level KAI1/CD82 inhibited polarized protrusion and retraction
38                                     Notably, KAI1/CD82 inhibits the formation of microprotrusions and
39                                       Hence, KAI1/CD82 interacts with tetraspanin and integrin by dif
40     The cancer metastasis suppressor protein KAI1/CD82 is a member of the tetraspanin superfamily.
41          Tumor metastases suppressor protein KAI1/CD82 is capable of blocking the tumor metastases wi
42 ive (+) cells, we found that the tetraspanin KAI1/CD82 is far more highly expressed in adult O4(+) ce
43 otility seen in the palmitoylation-deficient KAI1/CD82 mutant correlates with regaining of p130(CAS)-
44        Notably, the palmitoylation-deficient KAI1/CD82 mutant largely reversed the wild-type KAI1/CD8
45                      Moreover, we found that KAI1/CD82 palmitoylation affected motility-related subce
46                                              KAI1/CD82 protein is a member of the tetraspanin superfa
47 or motility are altered by KAI1/CD82 and how KAI1/CD82 regulates these events.
48                                     However, KAI1/CD82 still efficiently inhibits cell migration when
49  line Du145 was substantially inhibited when KAI1/CD82 was expressed.
50     In this study, we found that tetraspanin KAI1/CD82 was palmitoylated when expressed in PC3 metast
51 suggesting that the localized interaction of KAI1/CD82 with tetraspanin webs or tetraspanin-enriched
52 kII coupling, a signaling step important for KAI1/CD82's activity.
53 ion of these processes likely contributes to KAI1/CD82's inhibition of motility.
54 1/CD82 mutant largely reversed the wild-type KAI1/CD82's inhibitory effects on migration and invasion
55 panin-enriched microdomains is important for KAI1/CD82's motility-inhibitory activity.
56                                              KAI1/CD82, a tetraspanin protein, was first identified a
57                 To determine how tetraspanin KAI1/CD82, a tumor metastasis suppressor, inhibits cell
58                 Rac1 activity was reduced by KAI1/CD82, consistent with the diminution of lamellipodi
59 ctor-stimulated RhoA activity was blocked by KAI1/CD82, consistent with the loss of stress fiber and
60 ons maintain the conformational stability of KAI1/CD82, evidenced by the facts that the mutant is mor
61     Consistent with the wide distribution of KAI1/CD82, KASP is expressed ubiquitously in human tissu
62 eed important for the motility inhibition by KAI1/CD82, overexpression of p130CAS in Du145-KAI1/CD82
63 ion, homodimerization, and global folding of KAI1/CD82, the TM interactions maintain the conformation
64            In summary, we identified a major KAI1/CD82-associated protein, EWI2/PGRL, that is importa
65 sociated with KAI1/CD82 and named it KASP: a KAI1/CD82-associated surface protein.
66                                We found that KAI1/CD82-expressing cells typically exhibited elongated
67  FAK-Lyn-p130CAS-CrkII pathway is altered in KAI1/CD82-expressing cells, and 2) p130CAS-CrkII couplin
68 ame less detectable at the cell periphery in KAI1/CD82-expressing cells.
69                                    Moreover, KAI1/CD82-induced phenotypes likely resulted from the su
70 cur in the context of "tetraspanin web," the KAI1/CD82-KASP association is likely to be direct becaus
71 30CAS-CrkII complex and largely reversed the KAI1/CD82-mediated inhibition of cell motility.
72                             The mechanism of KAI1/CD82-mediated metastasis suppression remains unclea
73 ed protein, EWI2/PGRL, that is important for KAI1/CD82-mediated suppression of cancer cell migration.
74                             The mechanism of KAI1/CD82-mediated suppression of cancer metastasis rema
75 nd 2) p130CAS-CrkII coupling is required for KAI1/CD82-mediated suppression of cell motility.
76 nge are needed for the intrinsic activity of KAI1/CD82.
77 n-, and metastasis-suppressive activities of KAI1/CD82.
78 protein was decreased upon the expression of KAI1/CD82.
79  transmembrane proteins that associates with KAI1/CD82.
80 /PGRL is likely required for the function of KAI1/CD82.
81 n in breast cancer, we transfected the human KAI1 cDNA into two highly malignant breast cancer cell l
82 y compromised in DARC knockout mice, whereas KAI1 completely abrogated pulmonary metastasis in wild-t
83 r, in vitro and in vivo studies identify the KAI1-DARC interaction as a potential target for cancer t
84 biquitin-protein ligase gp78, a regulator of KAI1 degradation.
85  = 18), and cervix (n = 14) showed extensive KAI1 down-regulation.
86      We found no correlation between loss of KAI1 expression and stage of disease.
87     We also investigated the relationship of KAI1 expression and two other transmembrane four superfa
88                                      Reduced KAI1 expression associates with malignant progression of
89 lls expressing KAI1, whereas cells that lost KAI1 expression can proliferate, potentially giving rise
90 strated the utility of our assay by studying KAI1 expression in 34 lymphoid and 57 squamous lesions.
91 lish an immunohistochemical method to detect KAI1 expression in archival tissues.
92 istry is a suitable technique for evaluating KAI1 expression in archival tissues; (ii) KAI1 was not e
93  The purpose of our study was to investigate KAI1 expression in the progression of human colorectal c
94        In 10 patients, we also noted loss of KAI1 expression in the transition from normal colonic mu
95 was accompanied with significant decrease in KAI1 expression in vitro and in vivo.
96                                              KAI1 expression is decreased in the progression of commo
97                         To determine whether KAI1 expression is responsible for the metastasis suppre
98 a were significantly decreased while p53 and KAI1 expression levels were increased.
99                            Moreover, loss of KAI1 expression significantly abrogated NDRG1-mediated m
100                                 Furthermore, KAI1 expression significantly suppressed the in vitro ce
101                                         High KAI1 expression significantly suppressed the metastatic
102                                      Loss of KAI1 expression was also found in a subset of 10 high-gr
103        Previously, we have demonstrated that KAI1 expression was down-regulated in metastatic breast
104 31, which both have low levels of endogenous KAI1 expression.
105 we observed a progressive down-regulation of KAI1, from the normal adjacent colonic mucosa (KMS 193)
106                        The expression of the KAI1 gene also is found to be down-regulated during the
107 uppressor gene p53 can directly activate the KAI1 gene by interacting with the 5' upstream region.
108 sion of NDRG1 was able to augment endogenous KAI1 gene expression in prostate cancer cell lines, wher
109 gulatory mechanism for the expression of the KAI1 gene in human tissues.
110 gulatory mechanism for the expression of the KAI1 gene in normal and cancerous tissues, we characteri
111     The transcription initiation site of the KAI1 gene is located 181 bp upstream of the first nucleo
112 e tumors revealed that the expression of the KAI1 gene was correlated strongly to that of the p53 gen
113                                          The KAI1 gene, located on human chromosome 11p11.2, suppress
114 out 80 kb of DNA was identified as the human KAI1 gene, which contains 8 kb of 5'-region, 10 exons, 9
115  cancer, leads to the down-regulation of the KAI1 gene, which may result in the progression of metast
116 d transcription initiation site of the human KAI1 gene.
117 volve either mutation or allelic loss of the KAI1 gene.
118 hat ATF3 indeed bound to the promoter of the KAI1 gene.
119 TF3 expression followed by activation of the KAI1 gene.
120 dicate a direct relationship between p53 and KAI1 genes and suggest that the loss of p53 function, wh
121 ion of MMP-2, MMP-9, IL-1beta, p53, NM23 and KAI1 genes.
122                            Downregulation of KAI1 has been found to be clinically associated with met
123 (iii) there was extensive down-regulation of KAI1 in squamous cell carcinomas, suggestive of an impor
124 ment to the endothelial cell surface whereby KAI1 interacts with the Duffy antigen receptor for chemo
125                                              KAI1 is a metastasis suppressor gene for human prostate
126                                              KAI1 is a metastasis suppressor gene on human chromosome
127                                              KAI1 is a tumor metastasis suppressor gene that is capab
128                                Surprisingly, KAI1 is also directly activated by a ternary complex, de
129                  Using cell lines with known KAI1 levels and paraffin-embedded KAI1 positive tissues
130                                              KAI1 may also have post-translational modifications spec
131  melanocytes by Western blot to determine if KAI1 may be involved in multiple cancers.
132                   Our results suggested that KAI1 may function as a negative regulator of breast canc
133           Each tissue section was assigned a KAI1 mean score (KMS) from 0 to 300 based on the product
134            Decreased expression of the human KAI1 metastasis-suppressor gene is involved in the progr
135 nking each exon of KAI1 were used to analyze KAI1 mutation and allelic loss by the method of PLR-sing
136 five of 13 diffuse large cell lymphomas were KAI1 negative.
137         To evaluate whether dysregulation of KAI1 occurs during the progression of human prostatic ca
138      We conclude that the down-regulation of KAI1 occurs early in the progression of colorectal cance
139 mical analysis showed that loss of NDRG1 and KAI1 occurs in parallel as prostate cancer progresses.
140 with known KAI1 levels and paraffin-embedded KAI1 positive tissues as controls, we observed strong me
141          All eight reactive lymph nodes were KAI1 positive.
142           Further analysis revealed that the KAI1 promoter contained a consensus binding motif of ATF
143 epressor of gene transcription with LRP1 and KAI1 promoters.
144 immunohistochemical staining, high levels of KAI1 protein are detected in the epithelial but not stro
145 ndometrial cells had distinct, heterogeneous KAI1 protein band patterns in Western blots that were du
146                         We also investigated KAI1 protein expression by immunohistochemistry in tissu
147               These results demonstrate that KAI1 protein expression is consistently down-regulated d
148                                              KAI1 protein expression is downregulated in more than 70
149 ncers had downregulation, with 60% having no KAI1 protein expression.
150                                  We analysed KAI1 protein in normal and cancer cells of the prostate,
151 lung and pancreatic cancers, but the role of KAI1 protein in the malignant progression of other human
152                         In epithelial cells, KAI1 protein is expressed on the plasma membrane.
153                            Downregulation of KAI1 protein may be an indicator of metastatic potential
154  such untreated patients, down-regulation of KAI1 protein occurred in all of the lymph node metastase
155                                We found that KAI1 protein was downregulated in 31/42 of the cancer ce
156 ular mechanism of the suppressor function of KAI1 remains elusive.
157                            Overexpression of KAI1 results in metastasis suppression in certain highly
158      Our model of the mechanism of action of KAI1 shows that metastasis suppressor activity can be de
159         Here we report that tetraspanin CD82/KAI1 specifically suppresses ubiquitylation of EGFR afte
160 45 cells appears independent of p53, pRB and KAI1 status.
161 nteraction with host tissue and explains how KAI1 suppresses metastasis without affecting primary tum
162 ulated genes, exemplified by the tetraspanin KAI1 that regulates membrane receptor function.
163 -based analysis revealed that ATF3 modulated KAI1 transcription through cooperation with other endoge
164      Parental, vector-only transfectants and KAI1 transfectant clones were injected into the mammary
165 antly suppressed the metastatic potential of KAI1-transfected LCC6 cells.
166 tly suppressed the in vitro cell invasion in KAI1-transfected MDA-MB-231 cells.
167       In 84 patients with colorectal cancer, KAI1 was expressed at high levels in normal colonic muco
168                                              KAI1 was expressed heterogeneously, with the tumor cell
169                                              KAI1 was highly expressed in the primary SW480 colon can
170               The metastasis suppressor gene KAI1 was identified by its ability to inhibit the format
171 ng KAI1 expression in archival tissues; (ii) KAI1 was not expressed in a subset of both low-grade and
172 more, the metastasis-suppression activity of KAI1 was significantly compromised in DARC knockout mice
173 pha to the promoter of an APPct target gene (KAI1) was demonstrated.
174 loning, a metastatic suppressor gene, termed KAI1, was identified, which is located at human chromoso
175                          CD82, also known as KAI1, was recently identified as a prostate cancer metas
176         To define the mechanism of action of KAI1, we used a yeast two-hybrid screen and identified a
177 in expression, mutation, and allelic loss of KAI1 were analyzed using a tissue bank of 98 primary can
178 ved from the sequences flanking each exon of KAI1 were used to analyze KAI1 mutation and allelic loss
179  senescent signal to cancer cells expressing KAI1, whereas cells that lost KAI1 expression can prolif
180 f two metastasis suppressor genes, NDRG1 and KAI1, which together concerted metastasis-suppressive ac

 
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