Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Migration”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 757 records · Page 42Linked to original sources
PubMed1997

The migration of human smooth muscle cells in vitro is mediated by plasminogen activation and can be inhibited by alpha2-macroglobulin receptor associated protein.

The plasminogen activation system is thought to be important in cell migration processes. A role for this system during smooth muscle cell migration after vascular injury has been suggested from several animal studies. However, not much is known about its involvement in human vascular remodelling. We studied the involvement of the plasminogen activation system in human smooth muscle cell migration in more detail using an in vitro wound assay and a matrix invasion assay. Inhibition of plasmin activity or inhibition of urokinase-type plasminogen activator (u-PA) activity resulted in approximately 40% reduction of migration after 24 h in the wound assay and an even stronger reduction (70-80%) in the matrix invasion assay. Migration of smooth muscle cells in the presence of inhibitory antibodies against tissue-type plasminogen activator (t-PA) was not significantly reduced after 24 h, but after 48 h a 30% reduction of migration was observed, whereas in the matrix invasion assay a 50% reduction in invasion was observed already after 24 h. Prevention of the interaction of u-PA with cell surface receptors by addition of soluble u-PA receptor or alpha2-macroglobulin receptor associated protein (RAP) to the culture medium, resulted in a similar inhibition of migration and invasion. From these results it can be concluded that both u-PA and t-PA mediated plasminogen activation can contribute to in vitro human smooth muscle cell migration and invasion. Furthermore, the interaction between u-PA and its cell surface receptor appears also to be involved in this migration and invasion process. The inhibitory effects on migration and invasion by the addition of RAP suggests an involvement of a RAP sensitive receptor of the LDL receptor family, possibly the LDL-receptor related protein (LRP) and/or the VLDL receptor.

Cell Movement↗
PubMed1997

Tissue factor pathway inhibitor inhibits aortic smooth muscle cell migration induced by tissue factor/factor VIIa complex.

Tissue factor (TF), a transmembrane glycoprotein, forms a high affinity complex with factor VII/VIIa (FVIIa) and thereby initiates blood coagulation. Tissue factor pathway inhibitor (TFPI) is an endogenous protease inhibitor of TF/FVIIa-initiated coagulation. We previously reported that TF was a strong chemotactic factor for cultured vascular smooth muscle cells (SMCs). In this study, we examined the contribution of FVIIa and the effect of TFPI to TF-induced cultured SMC migration. TF/FVIIa complex showed a strong migration ability, however, neither TF alone nor FVIIa induced SMC migration. TF/FVIIa treated by a serine protease inhibitor and the complex of TF and inactivated FVIIa (DEGR-FVIIa) did not stimulate SMC migration. Pretreatment with hirudin and the antibodies to alpha-thrombin and factor X had no effect on TF/FVIIa-induced SMC migration, although alpha-thrombin and factor Xa also induced SMC migration respectively. TFPI markedly inhibited TF/FVIIa-induced SMC migration in a concentration-dependent manner, but did not affect the SMC migration induced by platelet-derived growth factor (PDGF)-BB, basic fibroblast-growth factor (bFGF), or alpha-thrombin. These results indicate that the catalytic activity of TF/FVIIa complex is important on SMC migration, and TFPI can reduce SMC migration as well as thrombosis.

Animals↗
PubMed1997

Adhesion and migration are differentially regulated in hematopoietic progenitor cells by cytokines and extracellular matrix.

The conditions that control the migratory status of hematopoietic progenitor cells on extracellular matrix (ECM) and that decide whether a cell migrates or adheres are incompletely understood. We analyzed the migratory behavior of murine hematopoietic progenitor cells factor-dependent-cell-paterson (FDCP)-mix and purified lin-Sca1+ bone marrow cells on ECM. We found that migration on fibronectin (Fn) or laminin (Lam) becomes dependent on beta1-integrins if a surface restraint force is introduced by tilting the ECM-coated culture vessels. Under these conditions, migration specifically occured on Fn and Lam, and was not detected on collagen IV-, hyaluronate-, or bovine serum albumin- coated surfaces. Migration depended on the continuous presence of hematopoietic cytokines interleukin-3 (IL-3), granulocyte colony-stimulating factor (G-CSF), macrophage-CSF (M-CSF), granulocyte-macrophage-CSF (GM-CSF), or stem cell factor (SCF), whereas other cytokines, such as IL-8, macrophage inflammatory protein-1alpha, macrophage-chemotactic and activating factor, and erythropoietin resulted in very little or no migratory response. IL-3 induced migration was synergistically enhanced by other CSFs, but was completely inhibited by addition of transforming growth factor-beta1. In contrast to firm local adhesion of previously cytokine depleted progenitors that was rapidly inducible within 1 hour after exposure to cytokines, preincubation on Fn matrix for 4 to 6 hours was required before cytokines could induce migration. A sudden increase of cytokine concentration reversibly inhibited migration and induced a fully adhesive state; this effect could be prolonged by consecutive stimulation with heterologous cytokines. Whereas cytokines activated resting progenitor cells to migrate on ECM, cell migration speed was regulated by Fn concentration. These results indicate that beta1-integrin-mediated progenitor cell adhesion and migration are differentially regulated by external stimuli and suggest that this regulation corresponds to different activation states of beta1-integrins in hematopoietic progenitor cells.

Animals↗
PubMedDate not supplied

A tumor derived motility factor that stimulates cell migration on extracellular matrix.

A factor that stimulates migration of lung carcinoma cells on biological substrata was purified from the human lung adenocarcinoma cell line WART. A partially purified autocrine motility factor-like substance, termed haptotaxin, was added to the lower compartment of Boyden chambers and the filters were coated on the upper, lower or both sides with different concentrations of the extracellular matrix (ECM) components fibronectin, laminin or collagen type IV. These adhesive proteins coated on the lower surface of the filter promoted the migration (haptotaxis) of lung carcinoma cells. This effect was greatly enhanced by the addition of haptotaxin. In contrast, ECM components (including gelatin) coated on the upper surface or on both filter surfaces did not stimulate tumor cell migration. However, the addition of haptotaxin also timulated cell migration under these conditions. Haptotaxin did not stimulate migration on filters coated with bovine serum albumin or on uncoated filters. Haptotaxin could not be absorbed by fibronectin, laminin, collagen type IV or gelatin, and soluble ECM components did not affect the locomotor effect of haptotaxin. Substrata coated with fibronectin, laminin and collagen type IV induced adhesion and spreading of lung carcinoma cells in a dose dependent fashion. Haptotaxin potentiated adhesion and spreading of tumor cells on these substrata but did not in itself mediate adhesion and spreading of the cells. Anti-VLA 2 antibodies inhibited migration to haptotaxin on gelatin and laminin coated filters but did not affect haptotaxin-induced migration on fibronectin or collagen type IV substrata. Anti-VLA-5 monoclonal antibodies inhibited haptotaxin-induced migration on fibronectin coated filters but not such migration on filters coated with other ECM molecules showing that tumor cells must interact specifically with ECM components in order to migrate to haptotaxin.

Adenocarcinoma↗
PubMed1985

Migration efficiency ratios and the optimal distribution of population.

The authors present a theoretical description of the migration process and criticize the conventional interpretation of the migration efficiency ratio, which is defined as the ratio of the net number of moves of individuals between areas to the gross number of moves that take place. "The conventional interpretation of the migration efficiency ratio is that the closer it lies to zero the less efficient the migration process....However, [the authors] feel that this is a somewhat misleading conception of the notion of efficiency in migration in that it emphasizes the physical efficiency of the migration process rather than focusing on the contribution of migration to a socially efficient allocation of population. Thus, to redirect attention, [they] have chosen to judge migration efficiency on the basis of its contribution to producing an equilibrium population distribution." The focus is on internal migration.

Demography↗
PubMed1991

Human-capital selectivity in interstate migration.

"Using Public Use Microdata Sample A from the 1980 United States Census, human capital measures are developed and used to test whether states experience human-capital migration that is significantly different from human migration. Strong evidence demonstrates that human-capital migration differs significantly from human migration. For example, Arkansas and Vermont are shown to have a net in-migration of people, but a net out-migration of human capital. Conversely, the data for Connecticut and Minnesota indicate a net out-migration of people and a net in-migration of human capital. This study suggests that traditional models of interstate migration mask the flow of human capital."

Americas↗
PubMed1998

Family interaction and migration decision making.

Using data from the Residential Preference and Migration Survey, a panel study of Pennsylvania households on migration intention and behavior, the authors examine some aspects of the decision to migrate. "We first examine the impact of the presence or absence of household interaction on the desire to move, migration expectations, and actual migration behavior. We hypothesize that the presence of household interaction is associated with migration behavior, while the absence of household interaction on migration-related issues is a predictor of staying in the present residence. Second, we test an expanded residential satisfaction migration decision model.... The expanded model permits us to test the thesis that household interaction frequency and consensus/conflict are moderating factors in explaining and predicting the outcome of migration decision making."

Americas↗
PubMed1987

L-fucose, D-mannose, L-galactose, and their BSA conjugates stimulate macrophage migration.

The effect of selected monosaccharides on the random migration of normal adult rabbit alveolar macrophages (AM) was investigated. It was observed that 10 mM of L-fucose, L-galactose, or D-mannose stimulated AM migration 1.5-2.0 times. In addition, derivatives of L-fucose and D-mannose occupying the carbon-6 position such as L-fucosyl-lactose, D-mannose-6-phosphate, D-mannitol, and mannan enhanced the migration of AM, whereas derivatives of L-fucose and D-mannose in the carbon-1 position produced no migration enhancement. Macrophage migration enhancement activity that was produced spontaneously by spleen cell cultures from normal young rabbits was destroyed by treatment with L-fucosidase. Accordingly, the migration enhancement factor (MEF) found in spleen cell culture supernatants appeared to depend on L-fucose conjugated to some protein carrier because MEF was non-dialyzable. When normal adult AM were treated with L-fucosidase, they lost their responsiveness to migration inhibitory factor (MIF) but retained their responsiveness to MEF. We have interpreted this to mean that the MIF and MEF receptors are distinct. Synthetic MEFs were prepared by conjugating L-fucose, D-mannose, of L-galactose to bovine serum albumin (BSA). It was noted that these sugar-BSA conjugates were about 200 times more effective than the corresponding free sugars in producing migration enhancement. In addition, these sugar-BSA conjugates neutralized MIF activity in a migration inhibition test.

Animals↗
PubMed1989

Effects of serum from human subjects of different ages on migration in vitro of human fibroblasts.

A study was carried out to determine whether human serum from older subjects inhibited cell migration. Sera of both sexes from subjects in their 60s (60-64 years) tended to be more inhibitory (8-14%) to the migration of human fetal lung fibroblasts, TIG-1, than serum from subjects in their 20s (20-29 years). In the case of females, the effects of serum on cell migration were significantly (P less than 0.05) different between the younger and older groups. Next, cell migration-stimulatory activity of serum was measured using human skin fibroblasts from young adult (age 21) and elderly (age 65) donors. The results were similar to those obtained with TIG-1 cells. However, the cell migration-stimulatory activity of serum was not significantly different between the two age groups. A study on the effects of concentration of human serum on the migration of TIG-1 cells showed that cell migration-stimulatory activity of serum declined linearly with increasing concentrations of sera from subjects in their teens (16-19 years) and 50s (50-59 years), and was the same between the two age groups. These results imply that substance(s) inhibitory to cell migration may not have accumulated in serum during the ageing process in humans, although human serum contained substance(s) inhibitory to cell migration.

Adolescent↗
PubMed1998

Intracranial migration of microplates versus wires in neonatal pigs after frontal advancement.

Several case reports have demonstrated that microplates migrate intracranially when used in the reconstruction of the neonatal craniofacial skeleton. We conducted a study to analyze the validity of this finding, to calculate the rate of intracranial plate migration, and to compare the migration of microplates to standard surgical wire. We hypothesized that, because of constant bone generation and resorption in the developing cranial skeleton, both microplates and wires would migrate and resorption in the developing cranial skeleton, both microplates and wires would migrate intracranially. Bilateral supraorbital osteotomies were performed in five 6-week-old Yucatan minipigs. The right side was repaired by fixating the bone segment with 32-gauge stainless steel wire. The left side was fixed with two microplates (Leibinger Corp, Dallas, TX). The pigs were monitored for 6 months. During this time each pig was injected with a fluorescent bone dye on the first day of each month. One pig was killed at 3 months and used for midpoint comparison. We found that both microplates and wires migrated intracranially in these neonatal pigs. None of the plates or wires penetrated the dura, but several pieces of hardware from each group migrated far enough to rest directly on the dural surface. The rate of plate and wire migration also varied slightly among animals, but the mean rate remained relatively constant at 0.91 mm/month. Computed tomographic scans and morphometric analysis revealed no significant difference between the fracture healing and facial growth of the microplate and wire sides. We conclude that the biology of bone deposition in the calvarium causes any stationary foreign body on the surface of the skull to migrate intracranially in the neonate.

Animals↗
PubMed1993

Potentiation and inhibition of migration of human neutrophils by auranofin.

OBJECTIVES: As auranofin resembles some neutrophil activating sulphur containing compounds, it was decided to investigate whether it had activating effects on neutrophil migration in addition to the published inhibitory effects. METHODS: The Boyden chamber assay was used to determine the migration velocity of human neutrophils. The difference between chemotaxis and chemokinesis was established with a chequerboard assay. RESULTS: Low concentrations of auranofin stimulated human neutrophil migration; concentrations of auranofin higher than 1 mumol/l were inhibitory. Inhibitors of leukotriene formation, or of protein kinase C, had the same effect on auranofin induced potentiation of migration as on fMLP activated migration. Auranofin, at a concentration of 100 nmol/l, caused a transient increase in the cGMP level of neutrophils. The auranofin induced increase in migration was strongly inhibited by methylene blue and by LY83583, two inhibitors of cGMP accumulation. CONCLUSIONS: The auranofin induced enhancement of migration is partly due to a chemokinetic effect, but mainly due to a chemotactic effect. The potentiating effect of auranofin on migration is not specifically due to the ability of the drug to inhibit protein kinase C activity or to generate leukotrienes. These results suggest that the enhancement of neutrophil migration by low levels of auranofin is related to the enhancement of cGMP levels in neutrophils.

Aminoquinolines↗
PubMed1988

Effect of parathyroid hormone on random migration of human polymorphonuclear leukocytes.

Derangements in leukocyte function occur in patients with primary hyperparathyroidism and in those with uremia, which is a state of secondary hyperparathyroidism, suggesting that parathyroid hormone (PTH) may affect leukocyte function. We examined the interaction between PTH and random migration of human polymorphonuclear leukocytes (PMNL) utilizing a modified Boyden chamber. Intact 1-84 PTH but not its amino-terminal (1-34 PTH) or its carboxy-terminal (53-84 PTH) fragments produced marked and significant (p less than 0.01) stimulation of random migration in a dose-dependent manner. Inactivation of 1-84 PTH abolished its effect and other peptide hormones (calcitonin, glucagon, insulin and vasopressin) did not stimulate migration of PMNL. The effect of PTH on migration was not due to action of the hormone on chemotaxis. PTH did not enhance cAMP or cGMP production by PMNL. The stimulation of PMNL motility by PTH was independent of calcium concentration in media, was not mimicked by calcium ionophore and was not blocked by verapamil. Quinidine also produced significant (p less than 0.01) increase in random migration of PMNL and this effect was not additive to that of PTH. Prolonged exposure to PTH (16-20 h) was associated with significant inhibition of random migration of PMNL. The migration of PMNL from patients with advanced renal failure was significantly (p less than 0.01) reduced and there was a significant (p less than 0.01) inverse relationship between random migration of PMNL and serum levels of PTH. Also PTH produced only modest stimulation of random migration of PMNL in most patients with renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Migration Inhibition↗
PubMed1977

Different concentrations of chemotactic factors can produce attraction or migration inhibition of leukocytes.

Parallel tests were conducted utilizing, the capillary tube migration test and the Boyden chamber assay, in order to determine whether the decrease in leukocyte chemotaxis that occurs if overoptimal cytotaxin concentrations are applied is due to migration inhibition. Overoptimal doses of casein produced decreased chemotactic response and migration inhibition for both rabbit macrophages and neutrophils. However, guinea pig neutrophils exhibited no decrease in chemotaxis despite high casein doses. Overoptimal doses of acid-denatured anaphylatoxin produced a decreased chemotactic response and migration inhibition of neutrophils. In both assays, this agent showed no effect upon macrophages. It is concluded that a chemotactic signal at different concentrations can elicit unidirectional migration or migration inhibition. Accordingly, chemotactic leukocyte attraction could be antagonistically regulated not only by serum-derived and lymphocyte-derived migration inhibitory factors but also by high doses of the chemotactic factor itself. Thus, the Boyden chamber technique can measure both chemotactic migration and migration inhibition phenomena.

Anaphylatoxins↗
PubMed2002

Stent-graft migration following endovascular repair of aneurysms with large proximal necks: anatomical risk factors and long-term sequelae.

PURPOSE: To evaluate the outcome of aortic endografts deployed in large infrarenal necks and to identify any association of preoperative aneurysm characteristics and postoperative morphological changes with the incidence of neck dilatation and device migration in this patient subset. METHODS: The records of 47 patients (41 men; mean age 74, range 55-84) with large aortic neck diameters treated with Talent stent-grafts from 1998 to 2001 were reviewed. Patients with anatomical criteria that precluded aneurysm exclusion with currently available devices were preferentially selected. Mean baseline aneurysm morphology included 27.6-mm (range 18-33.4) suprarenal and 28.1-mm (range 24-34) infrarenal neck diameters; the infrarenal neck length was 26 +/- 16 mm with angulation of 37 degrees +/- 18 degrees. Computed tomographic (CT) angiograms up to 3 years were analyzed using specialized interactive software; migration was defined as >1-cm change in the distance from the lower renal artery to the top of the device. Pre- and postoperative morphological characteristics of the aneurysm were compared between patients with and without migration. RESULTS: Of the 45 patients successfully treated, 40 had complete CT data for analysis. During a mean 17-month follow-up, 7 (17.5%) of the 40 devices exhibited distal migration. Six patients required secondary procedures; 5 were in the migration cohort. No preoperative anatomical characteristic or degree of neck dilatation over time was predictive of stent-graft migration. Aneurysm sac regression was significant at 1 (-0.09 +/- 4.90 mm) and 2 (-1.48 +/- 2.56 mm) years in endografts without migration (p<0.001). Distal endograft migration >1 cm predicted the need for secondary interventions (p<0.001), with 83% sensitivity and 94% specificity. CONCLUSIONS: Endovascular repair is successful in patients with large infrarenal necks and complex neck morphology. Changes in aneurysm remodeling over time were similar to reported observations in patients with more favorable neck criteria. Although no anatomical factor associated with migration could be identified from this analysis, distal displacement >1 cm correlated with the need for a secondary intervention.

Aged↗
PubMed1977

[Leucocyte migration inhibition test in diabetes mellitus (author's transl)].

The leucocyte migration inhibition test (LMT) using the agarose plate method introduced by Clausen is simple and highly reproducible. Using human pancreas extract and beef insulin as antigen, LMT was performed on ten patients with insulin dependent diabetes, twenty patients with insulin independent diabetes, and twelve healthy controls. The migration index was expressed as a percentage of migration calculated from the following formula. Migration index (MI) = average areas of migration in test suspension/average areas of migration in control suspension. Using human pancreas extract, the mean migration index for the insulin dependent diabetics (87.6 +/- 11.1) was significantly lower than in the normal subjects (99.3 +/- 6.3) (p less than 0.05). Using beef insulin as antigen for the insulin dependent diabetics and insulin independent diabetics, the mean migration indices (+/- SD) were 95.8 +/- 14.9 and 98.7 +/- 12.3 respectively. The corresponding values for the control group were 98.9 +/- 7.8. Cellular hypersensitivity to human pancreas extract was shown in the leucocyte migration inhibition test with insulin dependent diabetics, but a negative result was obtained with beef insulin.

Adult↗
PubMed2001

Functional caspase-1 is required for Langerhans cell migration and optimal contact sensitization in mice.

Langerhans cell (LC) migration from epidermis to draining lymph node is a critical first step in cutaneous immune responses. Both TNF-alpha and IL-1 beta are important signals governing this process, but the potential regulatory role of IL-1 alpha processing by caspase-1 is unknown. In wild-type (WT) mice, application of the contact allergens 2,4-dinitrofluorobenzine and oxazolone lead to a marked reduction in epidermal LC numbers, but in caspase-1-deficient mice this reduction was not observed. Moreover, although intradermal injection of TNF-alpha (50 ng) induced epidermal LC migration in WT mice, this cytokine failed to induce LC migration in caspase-1-deficient mice. Intradermal IL-1 beta (50 ng) caused a similar reduction in epidermal LC numbers in both WT and caspase-1-deficient mice, indicating that, given an appropriate signal, caspase-1-deficient epidermal LC are capable of migration. Contact hypersensitivity to both 2,4-dinitrofluorobenzine and oxazolone was inhibited in caspase-1-deficient mice, indicating a functional consequence of the LC migration defect. In organ culture the caspase-1 inhibitor Ac-YVAD-cmk, but not control peptide, potently inhibited the epidermal LC migration that occurs in this system, and reduced spontaneous migration of LC was observed in skin derived from caspase-1-deficient mice. Moreover, Ac-YVAD-cmk applied to BALB/c mouse skin before application of contact sensitizers inhibited LC migration and contact hypersensitivity in vivo. Taken together, these data indicate that caspase-1 may play a central role in the regulation of LC migration and suggest that the activity of this enzyme is amenable to control by specific inhibitors both in vivo and in vitro.

Administration, Cutaneous↗
PubMed2003

Intracellular domain of brain endothelial intercellular adhesion molecule-1 is essential for T lymphocyte-mediated signaling and migration.

To examine the role of the ICAM-1 C-terminal domain in transendothelial T lymphocyte migration and ICAM-1-mediated signal transduction, mutant human (h)ICAM-1 molecules were expressed in rat brain microvascular endothelial cells. The expression of wild-type hICAM-1 resulted in a significant increase over basal levels in both adhesion and transendothelial migration of T lymphocytes. Endothelial cells (EC) expressing ICAM-1 in which the tyrosine residue at codon 512 was substituted with phenylalanine (hICAM-1(Y512F)) also exhibited increased lymphocyte migration, albeit less than that with wild-type hICAM-1. Conversely, the expression of truncated hICAM-1 proteins, in which either the intracellular domain was deleted (hICAM-1DeltaC) or both the intracellular and transmembrane domains were deleted through construction of a GPI anchor (GPI-hICAM-1), did not result in an increase in lymphocyte adhesion, and their ability to increase transendothelial migration was attenuated. Truncated hICAM-1 proteins were also unable to induce ICAM-1-mediated Rho GTPase activation. EC treated with cell-permeant penetratin-ICAM-1 peptides comprising human or rat ICAM-1 intracellular domain sequences inhibited transendothelial lymphocyte migration, but not adhesion. Peptides containing a phosphotyrosine residue were equipotent in inhibiting lymphocyte migration. These data demonstrate that the intracellular domain of ICAM-1 is essential for transendothelial migration of lymphocytes, and that peptidomimetics of the ICAM-1 intracellular domain can also inhibit this process. Such competitive inhibition of transendothelial lymphocyte migration in the absence of an affect on adhesion further implicates ICAM-1-mediated signaling events in the facilitation of T lymphocyte migration across brain EC. Thus, agents that mimic the ICAM-1 intracellular domain may be attractive targets for novel anti-inflammatory therapeutics.

Animals↗
PubMed1999

Tyrosine phosphorylation of Crk-associated substrate lymphocyte-type is a critical element in TCR- and beta 1 integrin-induced T lymphocyte migration.

Crk-associated substrate (Cas) lymphocyte-type (Cas-L) is a 105-kDa cytoplasmic protein consisting of Src homology-3 domain and multiple YXXP motifs (substrate domain). Our previous studies showed that Cas-L is tyrosine-phosphorylated following the ligation of TCR and beta 1 integrins in T lymphocytes. Here we show that Cas-L is involved in T cell motility following the ligation of TCR and beta 1 integrin. Peripheral T lymphocytes showed a marked increase of migration on fibronectin (FN) after the ligation of TCR. In contrast, the migrating Jurkat cells, in which Cas-L was marginally expressed, were less than one-tenth in number on the same condition. Transfection of wild-type Cas-L into Jurkat cells resulted in restoring CD3 plus FN-induced cell migration. Furthermore, following the ligation of beta 1 integrin alone, the Cas-L transfectants significantly migrated better than the vector control. Mutational analysis of Cas-L revealed that the substrate domain is required for both FN- and CD3-induced tyrosine phosphorylation of Cas-L and cell migration caused by FN alone and CD3 plus FN. In contrast, the Src homology-3 domain is required only for the FN-induced tyrosine phosphorylation of Cas-L and cell migration, but not for CD3-induced tyrosine phosphorylation or CD3 plus FN-induced cell migration. These data strongly suggest that Cas-L is a key molecule in T cell migration induced by the ligation of CD3 and beta 1 integrins and that tyrosine phosphorylation of Cas-L is essential for T cell migration.

Adaptor Proteins, Signal Transducing↗