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Biomedical subjects

Lin Yang

Publications and source records attributed to Lin Yang.

At least 55 records · Page 3Linked to original sources
PubMed2006

Polymorphisms in the two helicases ERCC2/XPD and ERCC3/XPB of the transcription factor IIH complex and risk of lung cancer: a case-control analysis in a Chinese population.

The transcription factor IIH (TFIIH) helicases ERCC2/XPD and ERCC3/XPB are responsible for opening the DNA strand around the lesion site during nucleotide excision repair process. Genetic variants in these two genes may be markers for interindividual variability in DNA repair capacity and thus predisposition to cancer risk. In this case-control study of 1,010 incident lung cancer cases and 1,011 age and sex frequency-matched cancer-free controls in a Chinese population, we genotyped eight tagging polymorphisms of ERCC2 and ERCC3 using the high-throughput Taqman platform to determine their associations with risk of lung cancer. Although none of the eight polymorphisms was individually associated with lung cancer risk, we found that genetic variants in ERCC2 and ERCC3 jointly contributed to lung cancer risk in a dose-response manner. Compared with those with 0 to 1 "at-risk" locus, subjects carrying >1 at-risk loci were at increased risk for lung cancer [adjusted odds ratio (OR), 1.29; 95% confidence interval (95% CI), 0.98-1.70 for 2 at-risk loci; adjusted OR, 1.38; 95% CI, 1.02-1.85 for 3 at-risk loci; and adjusted OR, 1.51; 95% CI, 1.09-2.10 for > or =4 at-risk loci, respectively; P(trend) = 0.015]. This combined effect was slightly more evident in young subjects (<60 years), males, current smokers, and those with family history of cancer, particularly for histologic type of adenocarcinomas. No evidence for interaction was found. These findings indicate that these tagSNPs of the ERCC2 and ERCC3 along with their surrounding regions may serve as biomarkers of susceptibility to lung cancer, which warrant further validation by other population-based and phenotypic studies to determine the biological relevance of these tagSNPs.

Adenocarcinoma↗
PubMed2006

Cytotoxic synergy between the multikinase inhibitor sorafenib and the proteasome inhibitor bortezomib in vitro: induction of apoptosis through Akt and c-Jun NH2-terminal kinase pathways.

This study was undertaken to characterize preclinical cytotoxic interactions for human malignancies between the multikinase inhibitor sorafenib (BAY 43-9006) and proteasome inhibitors bortezomib or MG132. Multiple tumor cell lines of varying histiotypes, including A549 (lung adenocarcinoma), 786-O (renal cell carcinoma), HeLa (cervical carcinoma), MDA-MB-231 (breast), K562 (chronic myelogenous leukemia), Jurkat (acute T-cell leukemia), MEC-2 (B-chronic lymphocytic leukemia), and U251 and D37 (glioma), as well as cells derived from primary human glioma tumors that are likely a more clinically relevant model were treated with sorafenib or bortezomib alone or in combination. Sorafenib and bortezomib synergistically induced a marked increase in mitochondrial injury and apoptosis, reflected by cytochrome c release, caspase-3 cleavage, and poly(ADP-ribose) polymerase degradation in a broad range of solid tumor and leukemia cell lines. These findings were accompanied by several biochemical changes, including decreased phosphorylation of vascular endothelial growth factor receptor-2, platelet-derived growth factor receptor-beta, and Akt and increased phosphorylation of stress-related c-Jun NH2-terminal kinase (JNK). Inhibition of Akt was required for synergism, as a constitutively active Akt protected cells against apoptosis induced by the combination. Alternatively, the JNK inhibitor SP600125 could also protect cells from apoptosis induced by the combination, indicating that both inhibition of Akt and activation of JNK were required for the synergism. These findings show that sorafenib interacts synergistically with bortezomib to induce apoptosis in a broad spectrum of neoplastic cell lines and show an important role for the Akt and JNK pathways in mediating synergism. Further clinical development of this combination seems warranted.

Antineoplastic Agents↗
PubMed2006

[Study of cellular electrophysiology based on Noble98 dynamic model of ventricular action potential].

On the basis of mammalian ventricular action potential model Noble98, and with the use of Runge-Kutta for solution, the Wenckebach periodicity phenomenon, the transmural heterogeneity of the ventricular myocardium and its rate dependence are studied. The results indicate that these inherent properties may, lead to temporal-space disorganized in the normal heart,and may become the underlying factors for arrhythmias. At the same time, in this study are established the basic methods for quantitative cellular electrophysiology which is essential for future studies on the mechanism of arrhythmia.

Action Potentials↗
PubMed2006

[Relationship between VEGF and MMP-2, MMP-9 in 82 patients with acute myeloid leukemia].

In order to investigate the relationship between VEGF and matrix metalloproteinase (MMP)-2, -9 in acute myeloid leukemia patients, and evaluate the significance of them in extramedullary leukemic invasion, the expressions of MMP-2 mRNA, MMP-9 mRNA, VEGF mRNA in bone marrow from 86 patients with acute myeloid leukemia (AML), as well as human hematopoietic cell lines were analyzed by reverse transcription-polymerase chain reaction (RT-PCR). The proteolytic activities of MMP-2 and MMP-9 in the supernatants were measured by zymography. The VEGF protein in serum of all samples was detected by ELISA. All these results were analyzed for determination of the relationship between VEGF and MMP-2, MMP-9. The results showed that there was a positive correlation between expressions of MMP-2 mRNA or MMP-9 mRNA and VEGF mRNA or protein. But no such correlation was demonstrated in the AML (CR) and normal control (NC) groups. A higher expression level of MMP-2 and MMP-9 in the VEGF positive group was found, as compared with the negative group (P < 0.05). More extramedullary infiltration occurred in VEGF positive groups than that in VEGF negative groups of AML. The expression of bcl-2 in HL-60 cells was upregulated by VEGF. It is concluded that there are significantly positive correlations between the expression of MMP-2 and MMP-9 with VEGF mRNA or protein levels in AML patients. VEGF can upregulate the expression of MMP-2, MMP-9 in HL-60 and a part of the primary leukemic cells. VEGF and MMP-2, MMP-9 may participate in the extramedullary leukemic invasion of AML patients.

Adolescent↗
PubMed2006

[The effects of glutathione S-transferase (GSTT1 and GSTM1) genes polymorphisms on treatment efficacy and prognosis of acute myeloid leukemia].

OBJECTIVE: To investigate the impact of GSTT1 and GSTM1 genotypes on response, drug side effects and prognosis of acute myeloid leukemia (AML). METHODS: GSTT1 and GSTM1 genotypes were analysed in 180 AML patients with PCR. Complete remission (CR) rate, drug side-effects, overall survival, relapse-free survival and relapse rate were compared in groups with or without GSTT1 and GSTM1 genes. RESULTS: (1) The CR rate (96.9%) in GSTT1 and GSTM1 genes double-present patients was significantly higher than that in patients of GSTT1 null or GSTM1 null (CR rate 78.0%) (P = 0.013). The risk of failure to achieve CR in patients with GSTT1 null/GSTM1 null is 8.736 times higher than that in patients with GSTT1 and GSTM1 genes double-present (odds ratio OR was 8.736, 95% CI was 1.146 - 66.574). The CR rate (88.4%) in GSTT1 present patients was also significantly higher than that in patients of GSTT1 null (CR rate 74.7%) (P = 0.021, OR = 2.572, 95% CI 1.136 - 5.826). (2) There was no significant relationship between GSTT1/GSTM1 genotypes and the lasting time of neutrophilic granulocyte (ANC) < 0.5 x 10(9)/L and PLT < 20 x 10(9)/L. The risk of ALT abnormality in patients with GSTM1 null is 2.593 times higher than that in patients with GSTM1 present (P = 0.016, 95% CI 1.176 - 5.717). (3) Overall survival and relapse-free survival of GSTT1 and GSTM1 double-present patients were significantly better than those in patients of GSTT1 null/GSTM1 null (mean overall survival was 68.4 months vs 38.5 months, P = 0.028, and mean relapse-free survival was 73.5 months vs 34.9 months, P = 0.014, respectively). Relapse-free survival in GSTT1 null patients was significantly shorter than that in patients with GSTT1 present (26.7 months vs 64.3 months, P = 0.038), but there was no significant difference of overall survival between the two groups. The relapse rate of double-present patients was significantly lower than that of GSTT1 null/GSTM1 null patients (13.3% vs 35.6%, P = 0.019). CONCLUSION: GSTT1 and GSTM1 genotypes were apparently related with response, drug side effects and prognosis of patients with AML. GSTT1 and GSTM1 genotype might be useful in selecting appropriate chemotherapy regimens for patients with AML.

Adolescent↗
PubMed2006

[Computer simulation methods of cardiac electrophysiology].

Computer simulation is one of the powerful protocols to study electrophysiology theoretically. In this paper,the algorithm of Rush and Larsen was used to solve the ordinary differential equations (ODE's) in the Luo-Rudy models of mammalian ventricular cell. The operator splitting and adaptive time step methods were used to solve the partial differential equations (PDE's) in cardiac tissue conduction models. Using these methods we accomplished the simulation programs of single ventricular cell model and two-dimensional (2-D) tissue model. The methods of initiating spiral waves were studied with this software. The data obtained from 2-D simulation can be used for further study on isopotential contour lines, spiral wave tip trajectories, and pseudo-ECG.

Algorithms↗
PubMed2006

[Clinical and laboratory study of 4 cases of myelodysplastic syndromes with t (1;3) (p36; q21)].

OBJECTIVE: To study the clinical features of myelodysplastic syndromes (MDS) patients with t (1; 3) (p36; q21) and the expression of the involved genes. METHODS: 4 cases of MDS with t (1; 3) (p36; q21) were reported. The expression level of two transcription forms (PR-containing form MEL1 and PR-lacking form MEL1s) of MEL1 gene in normal fetus tissues, 2 healthy donor bone marrows and bone marrows from 3 MDS patients with t (1; 3) (p36; q21) were detected by semiquantitative reverse transcription polymerase chain reaction (RT-PCR). RESULTS: MDS patients with t (1; 3) (p36; q21) mainly presented with debility. Hemogram was macrocytic anemia, normal or elevated white blood cell and platelet counts. The bone marrow showed tri-lineage dysplasia especially dysmegakaryocytopoiesis. The patients had poor prognosis. MEL1 form was mainly expressed in the normal fetus tissues and healthy bone marrows, while the bone marrow cells from MDS patients with t (1; 3) (p36; q21) mainly or only expressed MEL1s. CONCLUSIONS: MDS patients with t (1; 3) (p36; q21) may be a new unique entity. Overexpression of MEL1s induced by t (1; 3) (p36; q21) might play an important role in the pathogenesis of this entity.

Aged↗
PubMed2006

[Randomized phase II trial on escalated doses of Rh-endostatin (YH-16) for advanced non-small cell lung cancer].

OBJECTIVE: To investigate the response rate (RR), time to tumor progression (TTP), quality of life (QOL) and adverse reaction in the treatment of pretreated advanced non-small cell lung cancer (NSCLC) using escalated doses of rh-endostatin (YH-16), and to determine the optimal dose for clinical application. METHODS: In this phase II randomized, controlled, multicenter trial, the patients were randomly divided into two groups to receive daily 3 hours intravenous infusion of either 7.5 mg x m(-2) or 15 mg/m(2) YH-16 for 28 days. RESULTS: Totally, 68 patients were entered and 60 patients were evaluable. There were no differences in RR (3.0% in both groups, P > 0.05), median TTP (ITT: 60 days versus 71 days, P > 0.05), QOL and incidence rate of adverse reactions (48.6% versus 38.7%, P > 0.05). No significant unexpected adverse events were observed. CONCLUSION: Rh-endostatin may have anti-tumor activity with high clinical benefit rate and is well tolerated in pretreated advanced NSCLC patients. The dose of 7.5 mg x (m(2))(-1) x d(-1) is clinically recommended.

Adolescent↗
PubMed2006

[Expression of midkine in patients with acute myeloid leukemia and its significance].

The study was aimed to investigate the expression of midkine (MK) in bone marrow mononuclear cells (BM MNC) from 65 acute myeloid leukemia patients and 15 normal controls. The method of RT-PCR was used to examine the expression of MK mRNA in BM MNC. Parts of samples were incubated for 24 hours and the gene expression of MK in the BM MNC was detected by means of Western blot. The results showed that the expression of MK of BM MNCs in 50 newly diagnosed AML patients (0.331 +/- 0.436) and 15 AML patients in relapse (0.374 +/- 0.463) were markedly higher than that in 15 CR cases (0.067 +/- 0.190), and 15 normal controls (0), respectively. The complete remission in MK positive patients (63.16%) was significantly lower than that in MK negative group (93.55%). The patients with positive MK expression had a higher relapse rate than those with negative MK expression. The positive rate of MK gene expression in drug-resistant patients and drug-sensitive patients were 57.69% and 25.64% respectively and there was positive correlation between the gene expressions of MK and bcl-2 (P < 0.01) (r = 0.0556, P < 0.001). It is concluded that MK can be secreted by AML cells and involved in drug-resistant, its positive expression may be associated with the poor prognosis in newly diagnosed AML patients. The inhibitory effect of MK on apoptosis of leukemic cells is induced by upregulating bcl-2 expression.

Adolescent↗
PubMed2006

WT1 gene expression lowered by IL-12 In vitro in peripheral blood mononuclear cells from patients with leukemia or myelodysplastic syndromes.

Previous studies demonstrated that interleukin-12 (IL-12) enhances the non-MHC-restricted cytotoxic activity of NK cells and facilitate specific allogeneic human cytotoxic T lymphocyte responses against fresh leukemia cells and cell lines. The Wilms' tumor gene, WT1 mRNA, has been used as a marker of minimal residual disease (MRD) for evaluating therapeutic efficacy of patients with leukemia or myelodysplastic syndrome (MDS). This study was aimed to investigate whether in vitro IL-12 can lower WT1 gene expression in peripheral blood monuclear cells (PBMNC) from patients with leukemia or MDS. PBMNC from these 30 patients and 5 healthy volunteers were cultured at 5 x 10(5) cells/ml alone with or without 100 units/ml of IL-12 for 3 days. WT1 mRNA was measured by competitive reverse transcription polymerase chain reaction (RT-PCR) since WT1 mRNA is considered as a marker of minimal residual disease (MRD) in leukemia and MDS. The results demonstrated that WT1 mRNA in PBMNC of 5 healthy volunteers was less than 10(3) copies/microg of total RNA. Following the 3-day IL-12 treatment, mean WT1 mRNA of PBMNC was reduced from 10(4.8) to 10(4.2) copies/microg of total RNA in 6 CML patients, from 10(5.4) to 10(4.8) copies/microg in 12 MDS patients and from 10(5.0) to 10(4.2) copies/microg in 5 AML patients in CR, but not reduced in 5 of 7 AML in non-CR. It is concluded that IL-12 significantly decrease the quantity of leukemia cells in PBMNC of most patients with MDS, CML and AML in CR. IL-12 may be of considerable benefit in the elimination of MRD in patients with hematological malignancies.

Adult↗
PubMed2006

[Effects of Astragalus injection on renal tubular function in patients with IgA nephropathy].

OBJECTIVE: To investigate the relationship between the renal tubular function and the severity of tubulo interstitial lesion and the effects of Astragalus Injection (AI) on renal tubular function in patients with IgA nephropathy (IgAN). METHODS: Sixty-seven patients with IgAN were randomly divided into the control group and the astragalus group, both received dipyridamole and benazepril orally, while the astragalus group treated with AI by intravenous dripping additionally. The indices for renal tubular function, including protein in blood and urine, urinary retinol binding protein (RBP) and N-acetyl-beta-D-glucosaminidase (UNAG), were detected. Area of glomerular Bowman capsule, renal tubules, and capillary were measured with color magic image analysis system type CMIAS2000. RESULTS: Urinary RBP and UNAG were correlated with tubulointerstitial lesion. Urine protein concentration decreased, blood albumin increased remarkably and renal tubular function improved after treatment in the astragalus group, with the improvement significantly different to those in the control group respectively. CONCLUSION: The severity of tubulointerstitial lesion was positively related to urinary RBP concentration, and astragalus injection has obvious effect on IgAN.

Adolescent↗
PubMed2006

[Down-regulation of Caspase-3 expression in precancerous lesions and its relation to gastric carcinogenesis].

OBJECTIVE: To study the level of expression of Caspase-3 protein in precancerous lesions of stomach and its relation to gastric carcinogenesis. METHODS: Formalin-fixed paraffin embedded tissues from 184 cases of gastric mucosa biopsy and surgically removed specimens, including gastric cancer (GC, N = 20), chronic atrophic gastritis (CAG, N = 6), atrophic gastritis with intestinal metaplasia (IM, N = 31), atrophic gastritis with dysplasia (DYS, N = 114) and normal controls (N = 13) were examined for expression of Caspase-3 protein and Ki-67 index by SABC immunohistochemistry, and for apoptosis by TdT-mediated dUTP biotin nick end labeling (TUNEL) method. Caspase-3, Ki-67 and TUNEL index were compared in different stages of gastric precancerous lesions and their correlation was analyzed. RESULTS: The positive index of Caspase-3 protein in severe DYS (29.8% +/- 3.9%) showed no significant difference compared with that in GC (26.9% +/- 3.0%, P > 0.05), but was significantly lower than that in low (58.3% +/- 4.2%) and moderate grade DYS (50.4% +/- 4.8%), CAG (68.3% +/- 3.3%) and IM (70.9% +/- 4.3%, P < 0.05). Caspase-3 positive index was significantly correlated with that of apoptosis detected by TUNEL (r = 0.94, P < 0.05). Ki-67 index in Caspase-3 protein positive group (18.3% +/- 2.2%) was significantly lower than that in Caspase-3 negative group (48.9% +/- 3.1%, P < 0.05). CONCLUSION: Caspase-3 protein expression was upregulated in CAG with or without IM and low or moderately low in DYS, while down-regulated in severe DYS and gastric carcinoma, and significantly positively correlated with cell apoptosis. It is suggested that down-regulated expression of Caspase-3 protein somehow contributes to gastric carcinogenesis through an imbalance between cell apoptosis and proliferation.

Adult↗
PubMed2006

[Determination of trace manganese by catalytic kinetic spectrophotometry method with CTMAB as the sensitizer].

A new catalytic spectrophotometric method for the determination of trace amount of Mn(II) was developed. The method is based on the oxidation of 7-(2-nitryl-4-methyl phenylazo)-8-hydroxy-qinolin-5-slfonic acid by potassium periodate in the presence of nitrilo triacec acid as an activator and CTMAB as a sensitizer. The wavelengths for the determination was 509 nm. The linear range of determination is 0-3. 2 x 10(-9) g x mL(-1) for Mn(II). The determination limit is 3.8 x 10(-11) g x mL(-1). The interference of foreign ions was studied. The method can be used for the determination of Mn(II) in mung bean, rice, cereal and soil samples.

English Abstract↗
PubMed2006

[Computer simulation study of the re-entry mechanisms in one-dimensional ischaemic myocardium].

Torsades de Pointes is a kind of severe ventricular arrhythmia. Myocardial ischaemia is one of the major causes leading to TdP. In this paper the mechanisms of the TdP were quantitatively studied under the condition of ischaemia based on the Noble98 dynamic model of the ventricular action potential. The study was conducted on one-dimensional homogeneous myocardium with the method of computer simulation. The models were firstly developed to simulate the lower excitability, extracellular accumulation of the K+ concentration or the decreased gap junctions in ischaemic myocardium. By separately reducing the Na+ conductance, increasing the extracellular K+ concentration or decreasing the conductance of the gap junctions enabled us to study the effect of each change in isolation. Then different degrees of ischaemic models were established to study their physiological features. The study showed that the conduction velocity became slower with the ischaemia aggravation, the action potential duration became shorter and the width of the vulnerable window obviously became larger than the normal conditions. The results illustrated that ischaemia was easily leading to unidirectional conduction block and resulted in re-entry and arrhythmias.

Computer Simulation↗
PubMed2006

[Study of nucleophosmin (NPM) gene mutation in patients with acute myeloid leukemia and myelodysplastic syndromes].

OBJECTIVE: To investigate nucleophosmin (NPM) gene mutations in patients with de novo acute myeloid leukemia (AML) with normal cytogenetics and primary myelodysplastic syndromes (MDS). METHODS: Genomic DNA corresponding to exon 12 of NPM gene was amplified by polymerase chain reaction (PCR) in 40 AML patients (28 case untreated and 12 in first remission) and 33 MDS patients. The PCR products were purified and screened by direct sequencing, the mutation PCR products were cloned into pUCm-T vector and then transfected into E. coil DH5alpha. At least 5 recombinant colonies were selected, and plasmid DNA were prepared and sequenced. RESULTS: NPM mutations were found in 6 patients (4 newly diagnosed AML and 2 MDS): 4 were type A,1 type B, and 1 novel sequence variant ( named as type R). CONCLUSION: A new type of NPM mutation was found, and NPM mutations in MDS patients were demonstrated for the first time. The results provides new hints for NPM gene mutations in the pathogenesis of AML and MDS.

Adolescent↗
PubMed2006

[Cross-sectional study of the relation between carboxypeptidase-H antibody and islet beta cell function in patients with latent autoimmune diabetes in adults].

OBJECTIVE: To explore the relation between carboxypeptidase-H antibody (CPH-Ab) and islet beta cell function in patients with latent autoimmune diabetes in adults (LADA) and to further confirm the diagnostic value of CPH-Ab for LADA. METHODS: Five hundred and forty-five patients who were initially diagnosed as Type 2 diabetes mellitus (T2DM) were tested with CPH-Ab and GAD-Ab by radioligand assay (RLA). T2DM patients, according to CPH-Ab and GAD-Ab status, were divided into CPH-Ab(+) group, GAD-Ab(+) group, and Ab(-) group to compare their islet beta cell function [represented by fasting C-peptide (FCP) and 2h postprandial C-peptide (2hCP)]. The relation between CPH-Ab and islet beta cell function in LADA was analyzed. RESULTS: The fasting C-peptide level in CPH-Ab(+) patients was between that of GAD-Ab(+) patients and that of Ab(-) patients (P<0.05), and the difference was still significant when the 3 groups were stratified with duration of disease (All P<0.05), but not with body mess index (all P>0.05). Corrected by concomitant variables including age, age at onset, duration of disease, and sex, the differences among the 3 groups were statistically significant (both P<0.001). Among the 3 groups FCP was lower than Ab(-) group in CPH-Ab(+) (P<0.05) and both FCP and PCP were lower than Ab(-) group in GAD-Ab(+) group (P<0.05 and P<0.01). The proportions of patients with insulin deficiency in CPH-Ab(+), GAD-Ab(+), and Ab(-) group were 27.6% (8/29), 48.1% (8/52) and 13.5% (54/400), respectively, which were significantly different among the 3 groups (P<0.001). GAD-Ab, BMI, and fasting blood glucose had effects on FCP and PCP in T2DM patients (All P<0.05), while CPH-Ab did not enter the equation in multivariable stepwise regressive analysis (P>0.05). CONCLUSION: The effect of CPH-Ab is less marked than that of GAD-Ab on islet beta-cell function in LADA patients. The value of CPH-Ab for the failure of islet beta-cell function in LADA should be determined prospectively.

Adult↗
PubMed2005

Endothelial cell cortactin phosphorylation by Src contributes to polymorphonuclear leukocyte transmigration in vitro.

The underlying mechanisms that regulate leukocyte transendothelial migration through the vascular endothelium remain unclear. Cortactin is a substrate of Src tyrosine kinases and a regulator of cytoskeletal dynamics. Previous studies demonstrated a role for Src phosphorylation of cortactin in clustering of E-selectin and intercellular cell adhesion molecule-1 around adherent leukocytes. In the current study, we used an in vitro flow model to investigate the role of Src-induced cortactin phosphorylation in endothelium during polymorphonuclear leukocyte (PMN) transmigration through human umbilical vein endothelium (HUVEC) monolayers preactivated with tumor necrosis factor-alpha. Inhibition of Src in HUVEC using Src kinase inhibitors PP2 and SU6656 reduced PMN transmigration by 45+/-8% and 36+/-6%, respectively. Live cell imaging of green fluorescent protein-tagged cortactin in HUVEC revealed redistribution of cortactin in the region surrounding transmigrating PMN. Knockdown of cortactin in HUVEC by small interfering RNA also impaired transmigration to a similar degree, and this phenotype was rescued by reexpression of wild-type cortactin. Analysis of the location of initial arrest and locomotion of PMN adherent to HUVEC demonstrated that inhibition of Src tyrosine kinases or pretreatment with cortactin small interfering RNA reduced PMN transmigration at endothelial cell-to-cell junctions and not adhesion. Tyrosine phosphorylation of cortactin was important for transmigration, because expression of a mutant, in which the tyrosine phosphorylation sites were mutated to phenylalanine (cortactin3F), failed to rescue PMN transmigration. Moreover, expression of cortactin3F alone partially blocked PMN transmigration. These data suggest a model whereby tyrosine phosphorylation of cortactin by Src family kinases regulates PMN transmigration.

Cell Adhesion↗