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1                                              JAM-A also is expressed on the surface of circulating he
2                                              JAM-A dimerization on a common cell surface (in cis) has
3                                              JAM-A is reported to contain N-glycans, but the extent o
4                                              JAM-A is required for establishment of viremia and viral
5                                              JAM-A is robustly expressed in normal human mammary epit
6                                              JAM-A localizes to tight junctions and contributes to pa
7                                              JAM-A or CD9 knockdown impairs endothelial cell migratio
8                                              JAM-A recruits Csk to the integrin-c-Src complex, where
9                                              JAM-A redistribution was associated with internalization
10                                              JAM-A serves many roles and contributes to barrier funct
11                                              JAM-A-deficient mice and cultured epithelial cells demon
12                                              JAM-A-deficient platelets showed increased aggregation a
13                                              JAM-C expressed on both murine B16 melanoma cells as wel
14                                              JAM-C expression was identified in human and murine mela
15                                              JAM-C has been implicated in leukocyte transendothelial
16                                              JAM-C inhibition significantly decreased the chemokine-i
17                                              JAM-C knockdown caused a delay in the hfRPE cell polariz
18                                              JAM-C localized at the tight junctions of cultured hfRPE
19                                              JAM-C localizes specifically in the tight junctions of h
20                                              JAM-C was also expressed on the surface of OA ST and RA
21                                              JAM-C was highly expressed by RA ST lining cells, and it
22                                              JAM-C(-/-) mice as well as endothelial-specific JAM-C-de
23           EC junctional adhesion molecule-1 (JAM-1), an alternative ligand for LFA-1, contributes exc
24 d in the HT-lo/diss variant, whereas NCAM-1, JAM-C, and TF levels were increased in the HT-hi/diss va
25 ndidates, four targets (i.e. TIMP-2, NCAM-1, JAM-C, and tissue factor (TF)) were selected for further
26 on the basal expression of TJ proteins ZO-1, JAM-2, Occludin, Claudin-3 and Claudin-5, using in vitro
27 ing in vivo differences in levels of TIMP-2, JAM-C, and TF were demonstrated in primary tumors grown
28                We have identified DHHC7 as a JAM-C palmitoylating enzyme by screening all known palmi
29 ohydrate and junctional adhesion molecule A (JAM-A) and internalization by beta1 integrin.
30  glycans and junctional adhesion molecule A (JAM-A) as attachment receptors.
31              Junctional adhesion molecule A (JAM-A) is a broadly expressed adhesion molecule that reg
32              Junctional adhesion molecule A (JAM-A) is a unique tight junction (TJ) transmembrane pro
33 , CLDN4, and junctional adhesion molecule A (JAM-A) subunits is induced at the GL.
34 PDZ3 ligand, junctional adhesion molecule A (JAM-A) to determine how the activity of different domain
35 irus engages junctional adhesion molecule A (JAM-A) to disseminate hematogenously.
36 recruited by junctional adhesion molecule A (JAM-A) to primordial junctions where aPKC is activated b
37              Junctional adhesion molecule A (JAM-A), a member of the cortical thymocyte marker of the
38 we show that junctional adhesion molecule A (JAM-A), a tight junction protein, is a key negative regu
39  proteins is junctional adhesion molecule A (JAM-A), an Ig fold transmembrane protein.
40 ace glycans, junctional adhesion molecule A (JAM-A), and the Nogo-1 receptor (depending on the cell t
41 1), CD99 and junctional adhesion molecule A (JAM-A), but apparently not vascular endothelial cell-spe
42 ttachment to junctional adhesion molecule A (JAM-A), virions undergo clathrin-mediated endocytosis fo
43 ohydrate and junctional adhesion molecule A (JAM-A).
44 ous receptor junctional adhesion molecule A (JAM-A).
45 Mice lacking junctional adhesion molecule A (JAM-A, encoded by F11r) exhibit enhanced intestinal epit
46 ins, such as junctional adhesion molecule-A (JAM)-A, occludin, and zonula occludens (ZO)-1.
47 ind to human Junctional Adhesion Molecule-A (JAM-A) and alpha4 integrin, respectively.
48  glycans and junctional adhesion molecule-A (JAM-A) and enters cells by receptor-mediated endocytosis
49 eceptors and junctional adhesion molecule-A (JAM-A) and is thought to undergo a conformational change
50 s: occludin, junctional adhesion molecule-A (JAM-A) and N-cadherin at the BTB.
51 e identify the junction adhesion molecule-A (JAM-A) as a key target for miR-34/449 in the developing
52              Junctional adhesion molecule-A (JAM-A) is a member of the immunoglobulin family with div
53              Junctional adhesion molecule-A (JAM-A) is a serotype-independent receptor for reovirus.
54              Junctional adhesion molecule-A (JAM-A) is a tight junction protein that serves as a rece
55              Junctional adhesion molecule-A (JAM-A) is a tight junction-associated signaling protein
56              Junctional adhesion molecule-A (JAM-A) is a TJ-associated protein that regulates barrier
57              Junctional adhesion molecule-A (JAM-A) is a transmembrane component of tight junctions t
58              Junctional adhesion molecule-A (JAM-A) is a transmembrane tight junction protein that ha
59              Junctional adhesion molecule-A (JAM-A) is an adherens and tight junction protein express
60 y shown that junctional adhesion molecule-A (JAM-A) renders protection from thrombosis by suppressing
61            Although we understand much about JAM-A, little is known regarding the protein's role in m
62 neage raised the possibility that additional JAM family paralogues may also function in muscle develo
63  permeability similar to that observed after JAM-A loss.
64  presence of neutralizing antibodies against JAM-C.
65 s, we generated strains of mice with altered JAM-A expression in these cell types and assessed bloods
66 tion proteins (occludin, claudin-5, ZO-1 and JAM-1) in the parenchymal blood vessels, as well as albu
67 tein down-regulation of ZO-1, claudin-5, and JAM-1 in HBMEC.
68 gnificant sub-functionalisation of JAM-B and JAM-C orthologues with respect to binding strength (but
69 the heterotypic adhesion molecules JAM-B and JAM-C.
70  engagement of cell-surface carbohydrate and JAM-A by the length and IDR mutant viruses.
71 junction proteins such as ZO-1, claudin, and JAM-A; however, exposure of SCs to inflammatory mediator
72 eased in the trJAM-A(-/-) apoe(-/-)mice, and JAM-A-deficient platelets showed increased binding to mo
73  also formed a stable complex with Pals1 and JAM-C (a component of the apical ES) in normal testes.
74  to the cell surface, reovirus particles and JAM-A codistribute into each of these compartments.
75 iously shown to be involved in angiogenesis (JAM-B and PTTG1IP), that, when overexpressed, are respon
76                            Accordingly, anti-JAM-C antibodies blocked adhesion of JAM-C-expressing B
77                            Neutralizing anti-JAM-C Abs inhibited RA synovial fluid-induced HMVEC chem
78             Long-term administration of anti-JAM-C antibodies prevented engraftment of JAM-Cpos lymph
79                          Treatment with anti-JAM-C antibodies in short-term experiments reduced migra
80                                    To assess JAM-A function in the lung, we depleted JAM-A in primary
81        We also show that integrin-associated JAM-A is tyrosine phosphorylated and is rapidly dephosph
82 method, that junctional adhesion molecule B (JAM-B) marks a previously unrecognized class of OFF RGCs
83 rin, ICAM-2, junctional adhesion molecule-B (JAM-B), laminin, and cellular fibronectin, supported bin
84                    A functional link between JAM-A and beta1 integrin was confirmed by restoration of
85  cell lines, an inverse relationship between JAM-A expression and the ability of these cells to migra
86      In addition, native MS analysis of bsAb/JAM-A immune complexes revealed that bsAb can bind up to
87 ued by inhibition of ROCK and phenocopied by JAM-A, JACOP, or p114RhoGEF down-regulation.
88 egrin, which responds to bFGF stimulation by JAM-A release to regulate mitogen-activated protein kina
89 xpression of junctional adhesion molecule C (JAM-C) at EC junctions, and they were enhanced by blocka
90  the role of junctional adhesion molecule C (JAM-C) in mediating leukocyte recruitment and retention
91              Junctional adhesion molecule C (JAM-C) is a transmembrane protein with significant roles
92              Junctional adhesion molecule C (JAM-C) is an immunoglobulin superfamily protein expresse
93              Junctional adhesion molecule C (JAM-C) is expressed by vascular endothelium and human bu
94 s, including junctional adhesion molecule-C (JAM-C) and myelin-associated glycoprotein (MAG).
95 e identified junctional adhesion molecule-C (JAM-C) as a novel player in melanoma metastasis to the l
96              Junctional adhesion molecule-C (JAM-C) is an adhesion molecule expressed at junctions be
97              Junctional adhesion molecule-C (JAM-C) is an adhesion molecule expressed by endothelial
98 ty of the EC junctional adhesion molecule-C (JAM-C).
99                        In endothelial cells, JAM-A has been implicated in basic fibroblast growth fac
100                                 In contrast, JAM-A deficiency in bone marrow cells impeded monocyte d
101         Compared to wild-type (WT) controls, JAM-C SC KO mice showed electrophysiological defects, mu
102     Overexpression of dimerization-defective JAM-A mutants in 293T cells inhibited cell spreading and
103 rt the effects of cis-dimerization-defective JAM-A mutants on epithelial cell migration and adhesion.
104      Protein phosphatase 2A dephosphorylates JAM-A at S285, suggesting that it antagonizes the activi
105 sess JAM-A function in the lung, we depleted JAM-A in primary alveolar epithelial cells using shRNA.
106 JAM-C-positive) and germinal center-derived (JAM-C-negative) B-cell lymphomas.
107 the classification of marginal zone-derived (JAM-C-positive) and germinal center-derived (JAM-C-negat
108 he Hz6F4 family preferentially binds dimeric JAM-A.
109 cycling to the membrane surface occur during JAM-A redistribution.
110 d vascular leakage, suggesting a role for EC JAM-C in the development of functional tumor vessels.
111  findings provide evidence for a role for EC JAM-C in tumor growth and aggressiveness as well as recr
112          However, tumor microvessels from EC JAM-C-deficient mice exhibited reduced pericyte coverage
113 , survival in this model was increased in EC JAM-C knockouts (KOs; 88 vs. 96 d, P=0.04) and reduced i
114 tumor growth was significantly reduced in EC JAM-C KOs (87% inhibition at 10 wk, P<0.0005), this was
115 (KOs; 88 vs. 96 d, P=0.04) and reduced in EC JAM-C transgenics (88 vs. 78.5 d, P=0.03), mice deficien
116             Local proteolytic cleavage of EC JAM-C by neutrophil elastase (NE) drove this cascade of
117 nt in promoting tumor growth, the role of EC JAM-C in tumor development was investigated using the ID
118 .03), mice deficient in or overexpressing EC JAM-C, respectively.
119                Our data identify endothelial JAM-A as an important effector molecule integrating athe
120 nt and luminal redistribution of endothelial JAM-A and were preferentially protected by its deficienc
121 expression and redistribution of endothelial JAM-A was increased by oxidized low-density lipoprotein,
122                    We found that endothelial JAM-A but not hematopoietic JAM-A facilitates reovirus T
123 M-A reveals that both sigma1 proteins engage JAM-A with similar affinities and via conserved binding
124 , but not a DHHC7 catalytic mutant, enhances JAM-C S-palmitoylation.
125                                     Finally, JAM-C promotes the basal-to-apical transmigration of gra
126 ngs identify N-glycosylation as critical for JAM-A's many functions.
127 ies identified JAM-B as the major ligand for JAM-C, whereas homotypic JAM-C interactions remained at
128 tetraspanin CD9 as novel binding partner for JAM-A in endothelial cells.
129 w that glycosylation of N185 is required for JAM-A-mediated reduction of cell migration.
130 iles and gene expression data generated from JAM-C-expressing leukemic cells, we defined a single cel
131 derlying cause of these defects, nerves from JAM-C SC KO mice were found to have morphological defect
132                         Cell adhesion genes, JAM-A and FSCN1, were downregulated with overexpression
133 ntributions of endothelial and hematopoietic JAM-A to reovirus dissemination and pathogenesis, we gen
134 that endothelial JAM-A but not hematopoietic JAM-A facilitates reovirus T1L bloodstream entry and egr
135 he major ligand for JAM-C, whereas homotypic JAM-C interactions remained at background levels.
136                                     However, JAM-A is dispensable for reovirus replication in the CNS
137                           We show that human JAM-A contains a single N-glycan at N185 and that this r
138         Plasmon resonance studies identified JAM-B as the major ligand for JAM-C, whereas homotypic J
139                         Our results identify JAM-C as a key regulator of polarized neutrophil TEM in
140                        We show that impaired JAM-A expression in endothelial cells reduced mononuclea
141 omatic or endothelium-specific deficiency in JAM-A and bone marrow chimeras with JAM-A-deficient leuk
142 ls after overexpression of beta1 integrin in JAM-A dimerization-defective cells.
143 icated involvement of RhoA and Rho kinase in JAM-A relocalization.
144 hemokine (C-C motif) ligand 2 (CCL2) induced JAM-A redistribution from the interendothelial cell area
145                By ~20 min, most internalized JAM-A moved to the brain endothelial cell apical membran
146  of JAM-C-expressing B cells to their ligand JAM-B, and immunofluorescence analysis showed the expres
147                   On alphaIIbbeta3 ligation, JAM-A was shown to be dephosphorylated, which could be p
148  binds to Junctional Adhesion Molecule-like (JAM-L) expressed on leukocytes.
149 gulates barrier; however, mechanisms linking JAM-A to epithelial permeability are poorly understood.
150 rowth factor (VEGF), respectively, CD9 links JAM-A specifically to alphavbeta3 integrin.
151 ts reduced migration of normal and malignant JAM-C-expressing B cells to bone marrow, lymph nodes, an
152                                The mammalian JAM family is composed of three cell surface receptors.
153  RPE (hfRPE) with or without si-RNA mediated JAM-C knockdown and in adult native RPE wholemounts.
154 r signature of J-RGCs, the adhesion molecule JAM-B, regulates morphogenesis, and showed that it promo
155 mined the role of the cell adhesion molecule JAM-C, a protein known to mediate cellular polarity duri
156                Junctional adhesion molecule (JAM)-A expressed in endothelial, epithelial, and blood c
157  In platelets, junctional adhesion molecule (JAM)-A was previously identified as an inhibitor of inte
158 , and for the heterotypic adhesion molecules JAM-B and JAM-C.
159 mite and that junctional adhesion molecules (JAMs) mediate this required Notch signal transduction.
160 ngs indicate that CD9 incorporates monomeric JAM-A into a complex with alphavbeta3 integrin, which re
161   CD9 interacts predominantly with monomeric JAM-A, which suggests that bFGF induces signaling by tri
162 anine substitutions to residues 43NNP45 (NNP-JAM-A) within the predicted trans-dimerization site did
163 revealed decreased association forces in NNP-JAM-A compared with WT and cis-null JAM-A.
164            Expression of nonphosphorylatable JAM-A/S285A interferes with single lumen specification d
165 n, antibodies against PECAM or CD99, but not JAM-A, block transcellular migration.
166      In contrast, beads coated with cis-null JAM-A demonstrated enhanced clustering similar to that o
167 d that expression of trans- but not cis-null JAM-A mutants decreased Rap2 activity.
168 s in NNP-JAM-A compared with WT and cis-null JAM-A.
169 ciated integral membrane proteins: occludin, JAM-A, and N-cadherin.
170                               The ability of JAM-A to attenuate cell invasion correlated with the for
171                                   Absence of JAM-A results in impaired c-SrcY(529) phosphorylation an
172 fection experiments revealed accumulation of JAM-A at sites between transfected cells, which was lost
173 y, anti-JAM-C antibodies blocked adhesion of JAM-C-expressing B cells to their ligand JAM-B, and immu
174 ighly migratory, express the least amount of JAM-A.
175 vely, the generation and characterization of JAM-C SC KO mice has provided unequivocal evidence for t
176                                  Deletion of JAM-A causes a gain-of-function in platelets, with lower
177  enhanced by blockade or genetic deletion of JAM-C in ECs.
178 ns further, mice with a specific deletion of JAM-C in SCs (JAM-C SC KO) were generated.
179                        Trans-dimerization of JAM-A may thus act as a barrier-inducing molecular switc
180 e results suggest that trans-dimerization of JAM-A occurs at a unique site and with different affinit
181   These results suggest that dimerization of JAM-A regulates cell migration and adhesion through indi
182 alization and expression after disruption of JAM-A dimerization suggested that internalization of bet
183 Last, we show that the functional effects of JAM dimerization require its carboxy-terminal postsynapt
184                     Assessment of effects of JAM-A dimerization on cell signaling revealed that expre
185    Notably, these proinflammatory effects of JAM-A-deficient platelets could be abolished by the inhi
186 ti-JAM-C antibodies prevented engraftment of JAM-Cpos lymphoma cells in bone marrow, spleen, and lymp
187 he HIV-induced decrease in the expression of JAM-A and occludin was restored by inhibition of MMP act
188 -NT did not alter cell surface expression of JAM-A or attachment of reovirus to cells.
189 ion of sigma1 and requires the expression of JAM-A.
190 th Afadin was dependent on the expression of JAM-A.
191 uorescence analysis showed the expression of JAM-B on murine and human lymphatic endothelial cells.
192 n, we recently reported on the expression of JAM-C in Schwann cells (SCs) and its importance for the
193  identify the localization and expression of JAM-C, ZO-1, N-cadherin, and ezrin in cultures of human
194 orts on previously undetected expressions of JAM-C, namely on perineural cells, and in line with noci
195          This study investigates the fate of JAM-A during inflammatory TJ complex remodeling and para
196 ggest a significant sub-functionalisation of JAM-B and JAM-C orthologues with respect to binding stre
197   To characterize cell-specific functions of JAM-A in atherosclerosis, we used apolipoprotein E-defic
198                           N-glycosylation of JAM-A is required for the protein's ability to reinforce
199     Finally, we show that N-glycosylation of JAM-A regulates leukocyte adhesion and LFA-1 binding.
200       We generated mice with inactivation of JAM-C.
201                                 Inclusion of JAM-C as a sole marker on lineage-negative BM cells yiel
202 ccelerate the kinetics of internalization of JAM-A, N-cadherin, and occludin versus controls.
203 GF-beta3-induced increase in the kinetics of JAM-A and occludin endocytosis was abolished, making the
204                    Furthermore, knockdown of JAM-A using short interfering RNAs enhanced the invasive
205                                 The level of JAM-C expression defines B-cell differentiation stages a
206 down decreases the S-palmitoylation level of JAM-C.
207 ratory MDA-MB-468 cells have lower levels of JAM-A on the cell surface.
208 AN nephrosis increased the protein levels of JAM-A, occludin, cingulin, and ZO-1 several-fold in glom
209 e least, are found to express high levels of JAM-A, whereas the more migratory MDA-MB-468 cells have
210                   In cultured cells, loss of JAM-A caused an approximately 30% decrease in transepith
211                         Furthermore, loss of JAM-A could be used as a biomarker for aggressive breast
212 stent with findings in other organs, loss of JAM-A decreased beta1 integrin expression and impaired f
213                        Additionally, loss of JAM-A resulted in elevated mucosal and serum IgA that wa
214                                      Loss of JAM-A, Afadin, or PDZ-GEF2, but not ZO-1 or PDZ-GEF1, si
215                            Overexpression of JAM-A in MDA-MB-231 cells inhibited both migration and i
216 ese results suggest that S-palmitoylation of JAM-C can be potentially targeted to control cancer meta
217                            Palmitoylation of JAM-C promotes its localization to tight junctions and i
218     Finally, we show that phosphorylation of JAM-A at Ser-284 is required for RhoA activation in resp
219 vely at the TJs, and S285 phosphorylation of JAM-A is required for the development of a functional ep
220 ly conserved Phe(-2) and Ser(-3) residues of JAM.
221 rge molecules, revealing a potential role of JAM-A in controlling perijunctional actin cytoskeleton i
222      These data demonstrate a direct role of JAM-A in mechanosignaling and control of RhoA and implic
223         These findings support a key role of JAM-A in promoting tight junction homeostasis and lung b
224 e present study, we investigated the role of JAM-C in homing of human B cells, using a xenogeneic non
225                     To determine the role of JAM-C in leukocyte retention in the RA synovium, in vitr
226                   To investigate the role of JAM-C in neuronal functions further, mice with a specifi
227      Our results highlight the novel role of JAM-C in recruiting and retaining leukocytes in the RA s
228    On injury, the enhanced susceptibility of JAM-A(-/-) mice to edema correlated with increased, tran
229 f de novo AML patients at diagnosis based on JAM-C-expressing cells frequencies in the blood served a
230  the apical surface, and it was dependent on JAM-A.
231 ST fibroblasts and to RA ST was dependent on JAM-C.
232             We found that tension imposed on JAM-A activates RhoA, which leads to increased cell stif
233 n fully polarized cells, S285-phosphorylated JAM-A is localized exclusively at the TJs, and S285 phos
234 inase (Csk) binds to tyrosine phosphorylated JAM-A through its Src homology 2 domain.
235 trongly suggest that tyrosine-phosphorylated JAM-A is a Csk-binding protein and functions as an endog
236 to primordial junctions, aPKC phosphorylates JAM-A at S285 to promote the maturation of immature cell
237    Our data suggest that aPKC phosphorylates JAM-A at S285 to regulate cell-cell contact maturation,
238 l interfering RNA oligonucleotides prevented JAM-A relocalization, suggesting that macropinocytosis a
239 on of p38 MAPK and of the junctional protein JAM-A.
240 aphragms contain the tight junction proteins JAM-A (junctional adhesion molecule A), occludin, and ci
241 itis (OA), and normal ST samples to quantify JAM-C expression.
242 ation of microRNA (miR)-145, which repressed JAM-A.
243 equivocal evidence for the involvement of SC JAM-C in the fine organization of peripheral nerves and
244 ce with a specific deletion of JAM-C in SCs (JAM-C SC KO) were generated.
245                                 Thus, sigma1-JAM-A interactions are unlikely to explain the differenc
246             Reovirus virions bind to soluble JAM-A and NgR1, while infectious disassembly intermediat
247 is found in soluble form and whether soluble JAM-C (sJAM-C) mediates angiogenesis.
248 lung, whereas treatment of mice with soluble JAM-C prevented melanoma lung metastasis.
249 bility and lesion formation, whereas somatic JAM-A deletion revealed no significant effects.
250 -C(-/-) mice as well as endothelial-specific JAM-C-deficient mice displayed significantly decreased B
251                    Upon agonist stimulation, JAM-A is dephosphorylated on the tyrosine, allowing the
252                                    Targeting JAM-C could thus constitute a new therapeutic strategy t
253 n the RA synovium and suggest that targeting JAM-C may be important in combating inflammatory disease
254 CD9 acts as scaffold and assembles a ternary JAM-A-CD9-alphavbeta3 integrin complex from which JAM-A
255                             We conclude that JAM-A normally limits platelet accumulation by inhibitin
256         We have previously demonstrated that JAM-A regulates cell migration by dimerization of the me
257                Finally, we demonstrated that JAM-C controls Src family kinase (SFK) activation in LSC
258                                We found that JAM-C is present in soluble form in normal serum and ele
259 hemical and structural studies indicate that JAM-A forms cis-homodimers, the functional significance
260                          Here we report that JAM-A associates directly with ZO-2 and indirectly with
261                         Here, we report that JAM-A is physically and functionally associated with the
262 ection of lipopolysaccharide, we report that JAM-A(-/-) mice showed increased susceptibility to pulmo
263                  In this study, we show that JAM-A associates with integrin alphaIIbbeta3 in resting
264                            Here we show that JAM-A in resting platelets functions as an endogenous in
265                        Our results show that JAM-C exists in soluble form and suggest that modulation
266                           Here, we show that JAM-C expression defines a subset of leukemic cells endo
267                           Here, we show that JAM-C undergoes S-palmitoylation on two juxtamembrane cy
268                  These findings suggest that JAM-A dimerization facilitates formation of a complex wi
269             Further experiments suggest that JAM-A does not regulate actin turnover but modulates act
270                   These results suggest that JAM-A regulates epithelial permeability via association
271 e cell migration, and evidence suggests that JAM-A may form homodimers between cells (in trans).
272             Analyses of cells expressing the JAM-A dimerization-defective mutant proteins revealed di
273 e head domain via epitopes distinct from the JAM-A-binding site.
274                       CAR is a member of the JAM family of adhesion receptors and is located to both
275  and in line with nociception defects of the JAM-C SC KO animals, on finely myelinated sensory nerve
276 SFK activation was uniquely found within the JAM-C-expressing LSC compartment.
277                                        Thus, JAM-A recruits Csk to the integrin-c-Src complex in rest
278                                        Thus, JAM-B identifies a unique population of RGCs in which st
279 nfectious subvirion particles, which bind to JAM-A but bypass a requirement for proteolytic uncoating
280 nding to only a few receptors: IE binding to JAM-B decreased with age, while binding to CD36 and inte
281 cture of serotype 3 reovirus sigma1 bound to JAM-A reveals that both sigma1 proteins engage JAM-A wit
282 core gene expression signature correlated to JAM-C expression that reveals LSC heterogeneity.
283 events as supported by presentation of NE to JAM-C via the neutrophil adhesion molecule Mac-1.
284 sassembly intermediates (ISVPs) bind only to JAM-A.
285                                    Together, JAM-C represents a novel therapeutic target for melanoma
286   Mice with or without platelet-specific (tr)JAM-A-deficiency in an apolipoprotein e (apoe(-/-)) back
287 ts that bFGF induces signaling by triggering JAM-A dimerization.
288  We also demonstrate that T1L/T3DM2 utilizes JAM-A more efficiently than T1L.
289 ) was efficacious at causing loss of venular JAM-C and promoting neutrophil reverse transendothelial
290 elial cell area to the apical surface, where JAM-A played a role as a leukocyte adhesion molecule par
291 n the current study, we investigated whether JAM-C is found in soluble form and whether soluble JAM-C
292 -CD9-alphavbeta3 integrin complex from which JAM-A is released upon bFGF stimulation.
293 iency in JAM-A and bone marrow chimeras with JAM-A-deficient leukocytes.
294      Of importance, microspheres coated with JAM-A containing alanine substitutions to residues 43NNP
295 F2 colocalized and coimmunoprecipitated with JAM-A.
296 ent protein sigma1 alone and in complex with JAM-A.
297 f association of the Par6/Pals1 complex with JAM-C, thereby destabilizing apical ES to facilitate spe
298 we show that aPKC can interact directly with JAM-A in a PAR-3-independent manner.
299 d that both antibodies likely interfere with JAM-A engagement by steric hindrance.
300 similar to that observed with wild-type (WT) JAM-A.

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