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Abl family kinases in development and disease

  • 125 Pages
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Landes bioscience/Springer Science+Business Media , New York, NY
Statement[edited by] Anthony J. Koleske.
Classifications
LC ClassificationsQP
The Physical Object
Pagination125 p. :
ID Numbers
Open LibraryOL22752539M
ISBN 139780387366401

Abl Family Kinases in Development and Disease (Molecular Biology Intelligence Unit): Medicine & Health Science Books @ agnesescriva.com Abl Family Kinases in Development and Disease provides an overview of the functions of Abl family kinases in Development and Disease.

This new title discusses the biochemical, genetic, and cell biological data that elucidate the cellular roles for these kinases in these. Abl Family Kinases in Development and Disease provides an overview of the functions of Abl family kinases in Development and Disease.

This new title discusses the biochemical, genetic, and cell biolog. Mechanisms of activation of Abl family kinases / Oliver Hantschel and Giulio Superti-Furga --Role of Abl family kinases in growth factor-mediated signaling / Ann Marie Pendergast --Regulation of cell adhesion responses by Abl family kinases / Keith Quincy Tanis and Martin Alexander Schwartz --Abl and cell death / Jean Y.J.

Wang, Yosuke Minami. Abl and Arg nonreceptor tyrosine kinases are widely expressed in mammals, where they contribute to the development of diverse organ and tissue systems. Deletion of abl or arg in mice reveals roles for the kinases in B and T lymphocyte development, neurulation, neuronal dendrite maintenance, synaptic plasticity, and osteoblast agnesescriva.com by: 1.

Description Abl family kinases in development and disease FB2

The vertebrate Abl family kinases, Abl and Arg, are expressed in the adult mouse brain, where they may regulate actin cytoskeletal dynamics in mature neurons. The Abl family of tyrosine kinases is regulated by a complex set of intramolecular interactions that impinge both directly and indirectly on the Abl kinase domain and lead to effective inhibition.

Chapter Three: Homeodomain-Interacting Protein Kinases: Diverse and Complex Roles in Development and Disease. Abstract. 1 Introduction. 2 Requirements for Hipk Proteins During Development. 3 Hipk Roles in Regulation of Diverse Signaling Pathways.

4 Regulation of Hipk Activity. 5 Hipks in Disease. 6 Conclusions. The Abelson (ABL) family of nonreceptor tyrosine kinases, ABL1 and ABL2, transduces Abl family kinases in development and disease book extracellular signals to protein networks that control proliferation, survival, migration, and invasion.

ABL1 was first identified as an oncogene required for the development of leukemias initiated by retroviruses or chromosome translocations. The demonstration that small molecule ABL kinase inhibitors effectively treat chronic myeloid leukemia Cited by: Jul 11,  · The Abelson (ABL) family of nonreceptor tyrosine kinases, ABL1 and ABL2, transduces diverse extracellular signals to protein networks that control proliferation, survival, migration and agnesescriva.com by: Home > Mechanisms of activation of Abl family kinases Editor(s): Koleske, Anthony J.

Published in: Abl family kinases in development and disease, Year: Publisher: New York, Springer. Swiss Institute for Experimental Cancer Research > UPHAN - Prof.

Hantschel Group Work outside EPFL Book chapters Published. Icon Cited by: 1. Jan 01,  · The Abelson tyrosine kinases were initially identified as drivers of leukemia in mice and humans.

The Abl family kinases Abl1 and Abl2 regulate diverse cellular processes during development and normal homeostasis, and their functions are subverted during inflammation, cancer and other pathologies. Abl kinases can be activated by multiple stimuli leading to cytoskeletal reorganization Cited by: Book Review (44) Book Chapter (28) Conference Proceeding (17) more Subjects.

Subjects. Sort by Item Count. Add All Remove All Filter by Abl Family Kinases in Development and Diseaseprovides an overview of the functions of Abl family kinases in Development and Disease.

The Src-family kinases (SFKs) are one such pathway and have been implicated in imatinib resistance. Additionally, these kinases are key to the progression of CML and Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL).Cited by: Jun 01,  · Abstract.

The Abl family of nonreceptor tyrosine kinases consists of two related proteins, c-Abl and Abl-related gene (Arg). Activated forms of the Abl kinases (BCR-Abl, Tel-Abl, and Tel-Arg) induce the development of human leukemia; it is not known, however, whether Abl kinases are activated in solid tumors or whether they contribute to tumor development or progression.

One such inhibitor is imatinib mesylate, which occupies the tyrosine kinase domain and inhibits BCR-ABL's influence on the cell cycle. Second generation BCR-ABL tyrosine-kinase inhibitors are also under development to inhibit BCR-ABL mutants resistant to agnesescriva.coms: ABL1, ABL proto-oncogene 1, non.

Feb 01,  · The Abelson tyrosine kinases were initially identified as drivers of leukemia in mice and humans. The Abl family kinases Abl1 and Abl2 regulate diverse cellular processes during development and normal homeostasis, and their functions are subverted Cited by: Dasatinib inhibits several multiple tyrosine kinases, including BCR-ABL and SRC family kinases, which are indicated for the treatment of adults with newly diagnosed chronic phase of CML.

Dasatinib exerts its anticancer effect through inhibiting several oncogenic tyrosine kinases such as BCR-ABL, expressed by Ph + stem cells, and is directly.

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The Abl family of non-receptor linked tyrosine kinases relay signals from diverse stimuli to promote changes in cell morphogenesis, migration, adhesion, proliferation and survival. Two Abl family kinases are found in vertebrates: Abl and the Abl-related gene (Arg, also known as Abl2) and homologs in metazoan organisms including Drosophila - (D.

Jan 01,  · The development of selective protein kinase inhibitors that can block or modulate diseases with abnormalities in these signaling pathways is considered a promising approach for drug development.

Because of their deregulation in human cancers, Bcr-Abl, EGFR, HER2, and protein kinase C (PKC), were among the first protein kinases considered as. The development of selective protein kinase inhibitors that can block or modulate diseases with abnormalities in these signaling pathways is considered a promising approach for drug development.

Because of their dereg-ulation in human cancers, Bcr-Abl, EGFR, HER2, and protein kinase C (PKC), were among the first protein. Sep 28,  · With the ongoing clinical success of the Bcr-Abl kinase inhibitor Gleevec in the treatment of chronic myelogenous leukemia and seven additional marketed kinase inhibitor drugs, researchers have compelling evidence that kinase inhibitors can be highly efficacious in the treatment of diseases caused by aberrant activity of protein kinase.

Oct 15,  · The ABL1 gene provides instructions for making a protein involved in many processes in cells throughout the body.

The ABL1 protein functions as a kinase, which is an enzyme that changes the activity of other proteins by adding a cluster of oxygen and phosphorus atoms (a phosphate group) at specific positions.

Kinase-Disease Associations As key regulators of most cellular pathways, protein kinases are frequently associated with diseases, either as causative agents or as therapeutic intervention points. We have summarized the disease research associations for over kinases. Nov 27,  · Common among those were the SRC, ABL and TEC family kinases.

Bosutinib did not inhibit KIT or platelet-derived growth factor receptor, but prominently targeted the apoptosis-linked STE20 kinases. Review Protein Kinases, Their Function and Implication in Cancer and Other Diseases (protein kinase / cancer therapy / protein phosphorylation) I.

SHCHEMELININ, L. ŠEFC, E. NEČAS Institute of Pathological Physiology and Centre of Experimental Haematology, 1st Faculty of Medicine, Charles University, Prague, Czech Republic Received June 29, nonreceptor tyrosine kinases and are closely related to the Src and Abl kinases (21, 22).

Functionally, Tec kinases play pivotal roles in the development and signaling of hematopoietic cells (23). Most notably, loss of Btk function is associated with the occurrence of X-linked agammaglobulinemia (XLA) character-ized by an impaired development Cited by: A greater understanding of the mechanisms that promote metastasis to the bone is required to identify actionable targets to treat this disease.

We have uncovered a novel role for the ABL family kinases in the regulation of breast cancer metastasis to the bone.

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The Abl kinases, Abl1 and Abl2, are a family of non-receptor tyrosine kinases that regulate a wide variety of cellular processes during development and normal homeostasis, but can have deleterious effects on cell survival, proliferation, and cell-cell junction adhesion upon their upregulation following inflammation, tumorigenesis, and oxidative stress.

The ErbB protein family or epidermal growth factor receptor (EGFR) family is a family of four structurally related receptor tyrosine kinases. Insufficient ErbB signaling in humans is associated with the development of neurodegenerative diseases, such as multiple sclerosis and Alzheimer's agnesescriva.com: BRENDA entry.

Abl kinases play a role in regulating the cytoskeleton and shape of a cell, proliferation and survival of the cell, cell adhesion, and cell migration (2, 3). Evidence has been reported that the protein of interest (POI) functions in development and signal transduction in the central nervous system of mice, as well as in mouse heart growth and.Abl Kinase.

The Abl family of non-receptor tyrosine kinases includes c-Abl (Abelson tyrosine kinase) and Arg (Abl2) subtypes. c-Abl is localized at many subcellular sites including the nucleus, cytoplasm, mitochondria and endoplasmic reticulum, where it interacts with several proteins.Apr 01,  · Using T-cell conditional knockout mice deficient for Abl family kinases, Abl (Abl1) and Abl-related gene (Arg) (Abl2), it was recently shown that loss of Abl kinases results in defective T-cell development and a partial block in the transition to the CD4(+)CD8(+) stage.