The Experts below are selected from a list of 513 Experts worldwide ranked by ideXlab platform
Pierre D. Mccrea - One of the best experts on this subject based on the ideXlab platform.
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ETV1 is a novel binding partner of Pkp3-catenin.
2014Co-Authors: William A. Munoz, Moonsup Lee, Malgorzata Kloc, Rachel K. Miller, Zamal Ahmed, Todd M. Link, Gilbert R. Lee, John E. Ladbury, Pierre D. MccreaAbstract:(A) Schematics of ETV1 and ETV5 protein structures. Red line indicates the binding region as suggested by sequenced prey clones identified from yeast-two hybrid screen. (B) Either HA-Pkp3 or HA-ARVCF was co-transfected with Myc-ETV1 in HEK 293T cells. Anti-Myc (ETV1) or –HA (Pkp3 or ARVCF) immune-precipitates were subjected to immuno-blotting with anti-Myc (ETV1) and –HA (Pkp3 or ARVCF) antibodies. Pkp3-catenin co-precipitates ETV1, but the structurally homologous ARVCF-catenin does not (negative/specificity control). ETV1 co-precipitates Pkp3, but does not co-precipitate ARVCF. (C) Untreated AB-1 wild type mouse embryonic stem cells were lysed and fractionated at 90% confluency and endogenous Pkp3 or ETV1 was immuno-precipitated from nuclear extracts, followed by immuno-blotting for Pkp3 and ETV1. Five percent inputs were acquired separately due to the low levels of endogenous proteins.
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JCB Article Vertebrate development requires ARVCF and p120 catenins and their interplay with RhoA and Rac
2013Co-Authors: Xiang Fang, Si Wan Kim, Jae Il Park, Travis G. Vaught, Panos Z. Anastasiadis, Malgorzata Ciesiolka, Pierre D. MccreaAbstract:Using an animal model system and depletion-rescue strategies, we have addressed the requirement and functions of armadillo repeat gene deleted in velo-cardio-facial syndrome (ARVCF) and p120 catenins in early vertebrate embryogenesis. We find that xARVCF and Xp120 are essential to development given that depletion of either results in disrupted gastrulation and axial elongation, which are specific phenotypes based on self-rescue analysis and further criteria. Exogenous xARVCF or Xp120 crossrescued depletion of the other, and each depletion was additionally rescued with (carefully titrated) dominant
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ARVCF depletion cooperates with tbx1 deficiency in the development of 22q11 2ds like phenotypes in xenopus
Developmental Dynamics, 2011Co-Authors: Hong Thi Tran, Pierre D. Mccrea, Mieke Delvaeye, Veerle Verschuere, Emilie Descamps, Ellen Crabbe, Luc Van Hoorebeke, Dominique Adriaens, Frans Van Roy, Kris VleminckxAbstract:The 22q11.2 deletion syndrome is a common dominant genetic disorder characterized by a heterozygous deletion of a cluster of genes on chromosome 22q11.2. TBX1, a transcription factor belonging to the T-box gene family, is a key player in the syndrome. However, heterozygosity of Tbx1 in mouse models does not fully recapitulate the phenotypes characteristic of the disease, which may point to the involvement of other genes in the deleted chromosomal region. Hence, we investigated the contribution of the catenin ARVCF, another gene that is deleted in 22q11.2DS. During Xenopus development, ARVCF mRNA is expressed in the pharyngeal arches and depleting either ARVCF or Tbx1 results in delayed migration of the cranial neural crest cells and in defects in the craniofacial skeleton and aortic arches. Moreover, double depletion of ARVCF and Tbx1 revealed that they act cooperatively, indicating that decreased ARVCF levels may also contribute to 22q11.2DS-associated phenotypes.
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ARVCF depletion cooperates with Tbx1 deficiency in the development of 22q11.2DS‐like phenotypes in Xenopus
Developmental dynamics : an official publication of the American Association of Anatomists, 2011Co-Authors: Hong Thi Tran, Pierre D. Mccrea, Mieke Delvaeye, Veerle Verschuere, Emilie Descamps, Ellen Crabbe, Luc Van Hoorebeke, Dominique Adriaens, Frans Van Roy, Kris VleminckxAbstract:The 22q11.2 deletion syndrome is a common dominant genetic disorder characterized by a heterozygous deletion of a cluster of genes on chromosome 22q11.2. TBX1, a transcription factor belonging to the T-box gene family, is a key player in the syndrome. However, heterozygosity of Tbx1 in mouse models does not fully recapitulate the phenotypes characteristic of the disease, which may point to the involvement of other genes in the deleted chromosomal region. Hence, we investigated the contribution of the catenin ARVCF, another gene that is deleted in 22q11.2DS. During Xenopus development, ARVCF mRNA is expressed in the pharyngeal arches and depleting either ARVCF or Tbx1 results in delayed migration of the cranial neural crest cells and in defects in the craniofacial skeleton and aortic arches. Moreover, double depletion of ARVCF and Tbx1 revealed that they act cooperatively, indicating that decreased ARVCF levels may also contribute to 22q11.2DS-associated phenotypes.
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Kazrin, and its binding partners ARVCF- and delta-catenin, are required for Xenopus laevis craniofacial development
Developmental dynamics : an official publication of the American Association of Anatomists, 2011Co-Authors: Kyucheol Cho, Moonsup Lee, Malgorzata Kloc, William A. Munoz, Pierre D. MccreaAbstract:The novel adaptor protein Kazrin associates with multifunctional entities including p120-subfamily members (ARVCF-, delta-, and p0071-catenin). Critical contributions of Kazrin to development or homeostasis are indicated with respect to ectoderm formation, integrity and keratinocyte differentiation, whereas its presence in varied tissues suggests broader roles. We find that Kazrin is maternally loaded, is expressed across development and becomes enriched in the forming head. Kazrin's potential contributions to craniofacial development were probed by means of knockdown in the prospective anterior neural region. Cartilaginous head structures as well as eyes on injected sides were reduced in size, with molecular markers suggesting an impact upon neural crest cell establishment and migration. Similar effects followed the depletion of ARVCF (or delta-catenin), with Kazrin:ARVCF functional interplay supported upon ARVCF partial rescue of Kazrin knockdown phenotypes. Thus, Kazrin and its associating ARVCF- and delta-catenins, are required to form craniofacial tissues originating from cranial neural crest and precordal plate.
En-hua Wang - One of the best experts on this subject based on the ideXlab platform.
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ARVCF expression is significantly correlated with the malignant phenotype of non-small cell lung cancer.
Molecular carcinogenesis, 2015Co-Authors: Di Zhang, Na Tang, Yang Liu, En-hua WangAbstract:Armadillo repeat gene deleted in velo-cardio-facial syndrome (ARVCF) is a member of the p120 catenin (p120ctn) family; it contains nine central Armadillo repeats and binds to the juxtamembrane domain of E-cadherin. We used immunohistochemistry to measure ARVCF expression in 121 patients with NSCLC and western blotting to examine differences in ARVCF expression between lung cancer and adjacent normal lung tissues. We interfered with ARVCF expression in two lung cancer cell lines and measured its effects on invasion and proliferation. ARVCF expression correlated with the malignant phenotype and poor prognosis. We also observed ARVCF-dependent changes in small GTPase (mainly RhoA) activity in lung cancer cells. We confirmed that ARVCF plays an important role in the malignant phenotype.
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ARVCF expression is significantly correlated with the malignant phenotype of non-small cell lung cancer.
Molecular Carcinogenesis, 2015Co-Authors: Di Zhang, Na Tang, Yang Liu, En-hua WangAbstract:Armadillo repeat gene deleted in velo-cardio-facial syndrome (ARVCF) is a member of the p120 catenin (p120ctn) family; it contains nine central Armadillo repeats and binds to the juxtamembrane domain of E-cadherin. We used immunohistochemistry to measure ARVCF expression in 121 patients with NSCLC and western blotting to examine differences in ARVCF expression between lung cancer and adjacent normal lung tissues. We interfered with ARVCF expression in two lung cancer cell lines and measured its effects on invasion and proliferation. ARVCF expression correlated with the malignant phenotype and poor prognosis. We also observed ARVCF-dependent changes in small GTPase (mainly RhoA) activity in lung cancer cells. We confirmed that ARVCF plays an important role in the malignant phenotype. © 2015 Wiley Periodicals, Inc.
Di Zhang - One of the best experts on this subject based on the ideXlab platform.
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ARVCF expression is significantly correlated with the malignant phenotype of non-small cell lung cancer.
Molecular carcinogenesis, 2015Co-Authors: Di Zhang, Na Tang, Yang Liu, En-hua WangAbstract:Armadillo repeat gene deleted in velo-cardio-facial syndrome (ARVCF) is a member of the p120 catenin (p120ctn) family; it contains nine central Armadillo repeats and binds to the juxtamembrane domain of E-cadherin. We used immunohistochemistry to measure ARVCF expression in 121 patients with NSCLC and western blotting to examine differences in ARVCF expression between lung cancer and adjacent normal lung tissues. We interfered with ARVCF expression in two lung cancer cell lines and measured its effects on invasion and proliferation. ARVCF expression correlated with the malignant phenotype and poor prognosis. We also observed ARVCF-dependent changes in small GTPase (mainly RhoA) activity in lung cancer cells. We confirmed that ARVCF plays an important role in the malignant phenotype.
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ARVCF expression is significantly correlated with the malignant phenotype of non-small cell lung cancer.
Molecular Carcinogenesis, 2015Co-Authors: Di Zhang, Na Tang, Yang Liu, En-hua WangAbstract:Armadillo repeat gene deleted in velo-cardio-facial syndrome (ARVCF) is a member of the p120 catenin (p120ctn) family; it contains nine central Armadillo repeats and binds to the juxtamembrane domain of E-cadherin. We used immunohistochemistry to measure ARVCF expression in 121 patients with NSCLC and western blotting to examine differences in ARVCF expression between lung cancer and adjacent normal lung tissues. We interfered with ARVCF expression in two lung cancer cell lines and measured its effects on invasion and proliferation. ARVCF expression correlated with the malignant phenotype and poor prognosis. We also observed ARVCF-dependent changes in small GTPase (mainly RhoA) activity in lung cancer cells. We confirmed that ARVCF plays an important role in the malignant phenotype. © 2015 Wiley Periodicals, Inc.
Yang Liu - One of the best experts on this subject based on the ideXlab platform.
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ARVCF expression is significantly correlated with the malignant phenotype of non-small cell lung cancer.
Molecular carcinogenesis, 2015Co-Authors: Di Zhang, Na Tang, Yang Liu, En-hua WangAbstract:Armadillo repeat gene deleted in velo-cardio-facial syndrome (ARVCF) is a member of the p120 catenin (p120ctn) family; it contains nine central Armadillo repeats and binds to the juxtamembrane domain of E-cadherin. We used immunohistochemistry to measure ARVCF expression in 121 patients with NSCLC and western blotting to examine differences in ARVCF expression between lung cancer and adjacent normal lung tissues. We interfered with ARVCF expression in two lung cancer cell lines and measured its effects on invasion and proliferation. ARVCF expression correlated with the malignant phenotype and poor prognosis. We also observed ARVCF-dependent changes in small GTPase (mainly RhoA) activity in lung cancer cells. We confirmed that ARVCF plays an important role in the malignant phenotype.
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ARVCF expression is significantly correlated with the malignant phenotype of non-small cell lung cancer.
Molecular Carcinogenesis, 2015Co-Authors: Di Zhang, Na Tang, Yang Liu, En-hua WangAbstract:Armadillo repeat gene deleted in velo-cardio-facial syndrome (ARVCF) is a member of the p120 catenin (p120ctn) family; it contains nine central Armadillo repeats and binds to the juxtamembrane domain of E-cadherin. We used immunohistochemistry to measure ARVCF expression in 121 patients with NSCLC and western blotting to examine differences in ARVCF expression between lung cancer and adjacent normal lung tissues. We interfered with ARVCF expression in two lung cancer cell lines and measured its effects on invasion and proliferation. ARVCF expression correlated with the malignant phenotype and poor prognosis. We also observed ARVCF-dependent changes in small GTPase (mainly RhoA) activity in lung cancer cells. We confirmed that ARVCF plays an important role in the malignant phenotype. © 2015 Wiley Periodicals, Inc.
Na Tang - One of the best experts on this subject based on the ideXlab platform.
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ARVCF expression is significantly correlated with the malignant phenotype of non-small cell lung cancer.
Molecular carcinogenesis, 2015Co-Authors: Di Zhang, Na Tang, Yang Liu, En-hua WangAbstract:Armadillo repeat gene deleted in velo-cardio-facial syndrome (ARVCF) is a member of the p120 catenin (p120ctn) family; it contains nine central Armadillo repeats and binds to the juxtamembrane domain of E-cadherin. We used immunohistochemistry to measure ARVCF expression in 121 patients with NSCLC and western blotting to examine differences in ARVCF expression between lung cancer and adjacent normal lung tissues. We interfered with ARVCF expression in two lung cancer cell lines and measured its effects on invasion and proliferation. ARVCF expression correlated with the malignant phenotype and poor prognosis. We also observed ARVCF-dependent changes in small GTPase (mainly RhoA) activity in lung cancer cells. We confirmed that ARVCF plays an important role in the malignant phenotype.
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ARVCF expression is significantly correlated with the malignant phenotype of non-small cell lung cancer.
Molecular Carcinogenesis, 2015Co-Authors: Di Zhang, Na Tang, Yang Liu, En-hua WangAbstract:Armadillo repeat gene deleted in velo-cardio-facial syndrome (ARVCF) is a member of the p120 catenin (p120ctn) family; it contains nine central Armadillo repeats and binds to the juxtamembrane domain of E-cadherin. We used immunohistochemistry to measure ARVCF expression in 121 patients with NSCLC and western blotting to examine differences in ARVCF expression between lung cancer and adjacent normal lung tissues. We interfered with ARVCF expression in two lung cancer cell lines and measured its effects on invasion and proliferation. ARVCF expression correlated with the malignant phenotype and poor prognosis. We also observed ARVCF-dependent changes in small GTPase (mainly RhoA) activity in lung cancer cells. We confirmed that ARVCF plays an important role in the malignant phenotype. © 2015 Wiley Periodicals, Inc.
