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Placing ion channels into a signaling network of T cells: from maturing thymocytes to healthy T lymphocytes or leukemic T lymphoblasts.

Dobrovinskaya O, Delgado-Enciso I, Quintero-Castro LJ, Best-Aguilera C, Rojas-Sotelo RM, Pottosin I - Biomed Res Int (2015)

Bottom Line: A new misdirecting "leukemogenic" signaling network appears, composed by three types of participants which are encoded by (1) genes implicated in determined stages of T cell development but deregulated by translocations or mutations, (2) genes which normally do not participate in T cell development but are upregulated, and (3) nondifferentially expressed genes which become highly interconnected with genes expressed differentially.In T cells, ion channels are implicated in regulation of cell cycle progression, differentiation, activation, migration, and cell death.In the present review we are going to reveal a relationship between different genetic defects, which drive the T cell neoplasias, with calcium signaling and ion channels.

View Article: PubMed Central - PubMed

Affiliation: Center for Biomedical Research, University of Colima, 28045 Colima, COL, Mexico.

ABSTRACT
T leukemogenesis is a multistep process, where the genetic errors during T cell maturation cause the healthy progenitor to convert into the leukemic precursor that lost its ability to differentiate but possesses high potential for proliferation, self-renewal, and migration. A new misdirecting "leukemogenic" signaling network appears, composed by three types of participants which are encoded by (1) genes implicated in determined stages of T cell development but deregulated by translocations or mutations, (2) genes which normally do not participate in T cell development but are upregulated, and (3) nondifferentially expressed genes which become highly interconnected with genes expressed differentially. It appears that each of three groups may contain genes coding ion channels. In T cells, ion channels are implicated in regulation of cell cycle progression, differentiation, activation, migration, and cell death. In the present review we are going to reveal a relationship between different genetic defects, which drive the T cell neoplasias, with calcium signaling and ion channels. We suggest that changes in regulation of various ion channels in different types of the T leukemias may provide the intracellular ion microenvironment favorable to maintain self-renewal capacity, arrest differentiation, induce proliferation, and enhance motility.

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Hierarchical mutagenesis during T cell maturation causes different types of T-ALL (see text for details).
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fig1: Hierarchical mutagenesis during T cell maturation causes different types of T-ALL (see text for details).

Mentions: It is widely accepted that T leukemogenesis is a multistep process where several genetic lesions drastically mislead the normal thymocyte maturation [2]. A short overview of key events in early thymocyte development and their links to the leukemogenesis is presented at Figure 1.


Placing ion channels into a signaling network of T cells: from maturing thymocytes to healthy T lymphocytes or leukemic T lymphoblasts.

Dobrovinskaya O, Delgado-Enciso I, Quintero-Castro LJ, Best-Aguilera C, Rojas-Sotelo RM, Pottosin I - Biomed Res Int (2015)

Hierarchical mutagenesis during T cell maturation causes different types of T-ALL (see text for details).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4383400&req=5

fig1: Hierarchical mutagenesis during T cell maturation causes different types of T-ALL (see text for details).
Mentions: It is widely accepted that T leukemogenesis is a multistep process where several genetic lesions drastically mislead the normal thymocyte maturation [2]. A short overview of key events in early thymocyte development and their links to the leukemogenesis is presented at Figure 1.

Bottom Line: A new misdirecting "leukemogenic" signaling network appears, composed by three types of participants which are encoded by (1) genes implicated in determined stages of T cell development but deregulated by translocations or mutations, (2) genes which normally do not participate in T cell development but are upregulated, and (3) nondifferentially expressed genes which become highly interconnected with genes expressed differentially.In T cells, ion channels are implicated in regulation of cell cycle progression, differentiation, activation, migration, and cell death.In the present review we are going to reveal a relationship between different genetic defects, which drive the T cell neoplasias, with calcium signaling and ion channels.

View Article: PubMed Central - PubMed

Affiliation: Center for Biomedical Research, University of Colima, 28045 Colima, COL, Mexico.

ABSTRACT
T leukemogenesis is a multistep process, where the genetic errors during T cell maturation cause the healthy progenitor to convert into the leukemic precursor that lost its ability to differentiate but possesses high potential for proliferation, self-renewal, and migration. A new misdirecting "leukemogenic" signaling network appears, composed by three types of participants which are encoded by (1) genes implicated in determined stages of T cell development but deregulated by translocations or mutations, (2) genes which normally do not participate in T cell development but are upregulated, and (3) nondifferentially expressed genes which become highly interconnected with genes expressed differentially. It appears that each of three groups may contain genes coding ion channels. In T cells, ion channels are implicated in regulation of cell cycle progression, differentiation, activation, migration, and cell death. In the present review we are going to reveal a relationship between different genetic defects, which drive the T cell neoplasias, with calcium signaling and ion channels. We suggest that changes in regulation of various ion channels in different types of the T leukemias may provide the intracellular ion microenvironment favorable to maintain self-renewal capacity, arrest differentiation, induce proliferation, and enhance motility.

Show MeSH
Related in: MedlinePlus