The Experts below are selected from a list of 63 Experts worldwide ranked by ideXlab platform

Craig C. Malbon - One of the best experts on this subject based on the ideXlab platform.

  • Constitutively active mutant GS alpha (G225T) and null-mutant G alpha i-2 (G203T) induce primitive endoderm from Stem Cells.
    American Journal of Physiology-Cell Physiology, 1995
    Co-Authors: Ping Gao, D. C. Watkins, Craig C. Malbon
    Abstract:

    In F9 teratocarcinoma Stem Cells, retinoic acid induces a primitive endoderm-like phenotype and a sharp decline in G alpha i-2, a response mimicked by expression of RNA antisense to G alpha i-2 in the absence of this morphogen (D. C. Watkins, G. L. Johnson, and C. C. Malbon. Science Wash. DC 258: 1373-1375, 1992). The role of the GS alpha/G alpha i-2 axis in cellular differentiation was explored. In the absence of retinoic acid, F9 Stem Cells stably expressing a constitutively active mutant of GS alpha (G225T) progressed to the primitive endoderm phenotype, as judged by morphological and differentiation markers, such as tissue plasminogen activator. Although elevated in Cells expressing G225T GS alpha, adenosine 39,59-cyclic monophosphate does not mimic retinoic acid action and alone fails to induce Stem Cells to primitive endoderm. In the absence of retinoic acid, expression of a null mutant of G alpha i-2 (G203T) also Induced Stem Cells to primitive endoderm. These observations establish G proteins in the GS alpha/G alpha i-2 axis as a control point for regulating progression to primitive endoderm independent of adenylate cyclase, in the present study9s model of early mouse development.

  • Constitutively active mutant Gsα (G22T) and null-mutant Gαi-2 (G203T) induce primitive endoderm from Stem Cells
    American Journal of Physiology-cell Physiology, 1995
    Co-Authors: Ping Gao, D. C. Watkins, Craig C. Malbon
    Abstract:

    Gao, Ping, David C. Watkins, and Craig C. Malbon. Constitutively active mutant G s α (G225T) and null-mutant Gα i-2 (G203T) induce primitive endoderm from Stem Cells. Am. J. Physiol. 268 (Cell Physiol. 37) : C1460-C1466, 1995.-In F9 teratocarcinoma Stem Cells, retinoic acid induces a primitive endoderm-like phenotype and a sharp decline in Gα i-2 , a response mimicked by expression of RNA antisense to Gα i-2 in the absence of this morphogen (D. C. Watkins, G. L. Johnson, and C. C. Malbon. Science Wash. DC 258 : 1373-1375, 1992). The role of the G s α/Gα i-2 axis in cellular differentiation was explored. In the absence of retinoic acid, F9 Stem Cells stably expressing a constitutively active mutant of G s α (G225T) progressed to the primitive endoderm phenotype, as judged by morphological and differentiation markers, such as tissue plasminogen activator. Although elevated in Cells expressing G225T Gas, adenosine 3',5'-cyclic monophosphate does not mimic retinoic acid action and alone fails to induce Stem Cells to primitive endoderm. In the absence of retinoic acid, expression of a null mutant of Gα i-2 (G203T) also Induced Stem Cells to primitive endoderm. These observations establish G proteins in the G s α/Gα i-2 axis as a control point for regulating progression to primitive endoderm independent of adenylate cyclase, in the present study's model of early mouse development.

Ping Gao - One of the best experts on this subject based on the ideXlab platform.

  • Constitutively active mutant GS alpha (G225T) and null-mutant G alpha i-2 (G203T) induce primitive endoderm from Stem Cells.
    American Journal of Physiology-Cell Physiology, 1995
    Co-Authors: Ping Gao, D. C. Watkins, Craig C. Malbon
    Abstract:

    In F9 teratocarcinoma Stem Cells, retinoic acid induces a primitive endoderm-like phenotype and a sharp decline in G alpha i-2, a response mimicked by expression of RNA antisense to G alpha i-2 in the absence of this morphogen (D. C. Watkins, G. L. Johnson, and C. C. Malbon. Science Wash. DC 258: 1373-1375, 1992). The role of the GS alpha/G alpha i-2 axis in cellular differentiation was explored. In the absence of retinoic acid, F9 Stem Cells stably expressing a constitutively active mutant of GS alpha (G225T) progressed to the primitive endoderm phenotype, as judged by morphological and differentiation markers, such as tissue plasminogen activator. Although elevated in Cells expressing G225T GS alpha, adenosine 39,59-cyclic monophosphate does not mimic retinoic acid action and alone fails to induce Stem Cells to primitive endoderm. In the absence of retinoic acid, expression of a null mutant of G alpha i-2 (G203T) also Induced Stem Cells to primitive endoderm. These observations establish G proteins in the GS alpha/G alpha i-2 axis as a control point for regulating progression to primitive endoderm independent of adenylate cyclase, in the present study9s model of early mouse development.

  • Constitutively active mutant Gsα (G22T) and null-mutant Gαi-2 (G203T) induce primitive endoderm from Stem Cells
    American Journal of Physiology-cell Physiology, 1995
    Co-Authors: Ping Gao, D. C. Watkins, Craig C. Malbon
    Abstract:

    Gao, Ping, David C. Watkins, and Craig C. Malbon. Constitutively active mutant G s α (G225T) and null-mutant Gα i-2 (G203T) induce primitive endoderm from Stem Cells. Am. J. Physiol. 268 (Cell Physiol. 37) : C1460-C1466, 1995.-In F9 teratocarcinoma Stem Cells, retinoic acid induces a primitive endoderm-like phenotype and a sharp decline in Gα i-2 , a response mimicked by expression of RNA antisense to Gα i-2 in the absence of this morphogen (D. C. Watkins, G. L. Johnson, and C. C. Malbon. Science Wash. DC 258 : 1373-1375, 1992). The role of the G s α/Gα i-2 axis in cellular differentiation was explored. In the absence of retinoic acid, F9 Stem Cells stably expressing a constitutively active mutant of G s α (G225T) progressed to the primitive endoderm phenotype, as judged by morphological and differentiation markers, such as tissue plasminogen activator. Although elevated in Cells expressing G225T Gas, adenosine 3',5'-cyclic monophosphate does not mimic retinoic acid action and alone fails to induce Stem Cells to primitive endoderm. In the absence of retinoic acid, expression of a null mutant of Gα i-2 (G203T) also Induced Stem Cells to primitive endoderm. These observations establish G proteins in the G s α/Gα i-2 axis as a control point for regulating progression to primitive endoderm independent of adenylate cyclase, in the present study's model of early mouse development.

D. C. Watkins - One of the best experts on this subject based on the ideXlab platform.

  • Constitutively active mutant GS alpha (G225T) and null-mutant G alpha i-2 (G203T) induce primitive endoderm from Stem Cells.
    American Journal of Physiology-Cell Physiology, 1995
    Co-Authors: Ping Gao, D. C. Watkins, Craig C. Malbon
    Abstract:

    In F9 teratocarcinoma Stem Cells, retinoic acid induces a primitive endoderm-like phenotype and a sharp decline in G alpha i-2, a response mimicked by expression of RNA antisense to G alpha i-2 in the absence of this morphogen (D. C. Watkins, G. L. Johnson, and C. C. Malbon. Science Wash. DC 258: 1373-1375, 1992). The role of the GS alpha/G alpha i-2 axis in cellular differentiation was explored. In the absence of retinoic acid, F9 Stem Cells stably expressing a constitutively active mutant of GS alpha (G225T) progressed to the primitive endoderm phenotype, as judged by morphological and differentiation markers, such as tissue plasminogen activator. Although elevated in Cells expressing G225T GS alpha, adenosine 39,59-cyclic monophosphate does not mimic retinoic acid action and alone fails to induce Stem Cells to primitive endoderm. In the absence of retinoic acid, expression of a null mutant of G alpha i-2 (G203T) also Induced Stem Cells to primitive endoderm. These observations establish G proteins in the GS alpha/G alpha i-2 axis as a control point for regulating progression to primitive endoderm independent of adenylate cyclase, in the present study9s model of early mouse development.

  • Constitutively active mutant Gsα (G22T) and null-mutant Gαi-2 (G203T) induce primitive endoderm from Stem Cells
    American Journal of Physiology-cell Physiology, 1995
    Co-Authors: Ping Gao, D. C. Watkins, Craig C. Malbon
    Abstract:

    Gao, Ping, David C. Watkins, and Craig C. Malbon. Constitutively active mutant G s α (G225T) and null-mutant Gα i-2 (G203T) induce primitive endoderm from Stem Cells. Am. J. Physiol. 268 (Cell Physiol. 37) : C1460-C1466, 1995.-In F9 teratocarcinoma Stem Cells, retinoic acid induces a primitive endoderm-like phenotype and a sharp decline in Gα i-2 , a response mimicked by expression of RNA antisense to Gα i-2 in the absence of this morphogen (D. C. Watkins, G. L. Johnson, and C. C. Malbon. Science Wash. DC 258 : 1373-1375, 1992). The role of the G s α/Gα i-2 axis in cellular differentiation was explored. In the absence of retinoic acid, F9 Stem Cells stably expressing a constitutively active mutant of G s α (G225T) progressed to the primitive endoderm phenotype, as judged by morphological and differentiation markers, such as tissue plasminogen activator. Although elevated in Cells expressing G225T Gas, adenosine 3',5'-cyclic monophosphate does not mimic retinoic acid action and alone fails to induce Stem Cells to primitive endoderm. In the absence of retinoic acid, expression of a null mutant of Gα i-2 (G203T) also Induced Stem Cells to primitive endoderm. These observations establish G proteins in the G s α/Gα i-2 axis as a control point for regulating progression to primitive endoderm independent of adenylate cyclase, in the present study's model of early mouse development.

Takayuki Nakagomi - One of the best experts on this subject based on the ideXlab platform.

  • Neural regeneration by regionally Induced Stem Cells within post-stroke brains: Novel therapy perspectives for stroke patients
    World journal of stem cells, 2019
    Co-Authors: Takayuki Nakagomi, Toshinori Takagi, Mikiya Beppu, Shinichi Yoshimura, Tomohiro Matsuyama
    Abstract:

    Neural regeneration by regionally Induced Stem Cells within post-stroke brains: Novel therapy perspectives for stroke patients

  • Novel Regenerative Therapies Based on Regionally Induced Multipotent Stem Cells in Post-Stroke Brains: Their Origin, Characterization, and Perspective
    Translational Stroke Research, 2017
    Co-Authors: Toshinori Takagi, Shinichi Yoshimura, Tomohiro Matsuyama, Rika Sakuma, Akiko Nakano-doi, Takayuki Nakagomi
    Abstract:

    Brain injuries such as ischemic stroke cause severe neural loss. Until recently, it was believed that post-ischemic areas mainly contain necrotic tissue and inflammatory Cells. However, using a mouse model of cerebral infarction, we demonstrated that Stem Cells develop within ischemic areas. Ischemia-Induced Stem Cells can function as neural progenitors; thus, we initially named them injury/ischemia-Induced neural Stem/progenitor Cells (iNSPCs). However, because they differentiate into more than neural lineages, we now refer to them as ischemia-Induced multipotent Stem Cells (iSCs). Very recently, we showed that putative iNSPCs/iSCs are present within post-stroke areas in human brains. Because iNSPCs/iSCs isolated from mouse and human ischemic tissues can differentiate into neuronal lineages in vitro, it is possible that a clearer understanding of iNSPC/iSC profiles and the molecules that regulate iNSPC/iSC fate (e.g., proliferation, differentiation, and survival) would make it possible to perform neural regeneration/repair in patients following stroke. In this article, we introduce the origin and traits of iNSPCs/iSCs based on our reports and recent viewpoints. We also discuss their possible contribution to neurogenesis through endogenous and exogenous iNSPC/iSC therapies following ischemic stroke.

Tomohiro Matsuyama - One of the best experts on this subject based on the ideXlab platform.

  • Neural regeneration by regionally Induced Stem Cells within post-stroke brains: Novel therapy perspectives for stroke patients
    World journal of stem cells, 2019
    Co-Authors: Takayuki Nakagomi, Toshinori Takagi, Mikiya Beppu, Shinichi Yoshimura, Tomohiro Matsuyama
    Abstract:

    Neural regeneration by regionally Induced Stem Cells within post-stroke brains: Novel therapy perspectives for stroke patients

  • Novel Regenerative Therapies Based on Regionally Induced Multipotent Stem Cells in Post-Stroke Brains: Their Origin, Characterization, and Perspective
    Translational Stroke Research, 2017
    Co-Authors: Toshinori Takagi, Shinichi Yoshimura, Tomohiro Matsuyama, Rika Sakuma, Akiko Nakano-doi, Takayuki Nakagomi
    Abstract:

    Brain injuries such as ischemic stroke cause severe neural loss. Until recently, it was believed that post-ischemic areas mainly contain necrotic tissue and inflammatory Cells. However, using a mouse model of cerebral infarction, we demonstrated that Stem Cells develop within ischemic areas. Ischemia-Induced Stem Cells can function as neural progenitors; thus, we initially named them injury/ischemia-Induced neural Stem/progenitor Cells (iNSPCs). However, because they differentiate into more than neural lineages, we now refer to them as ischemia-Induced multipotent Stem Cells (iSCs). Very recently, we showed that putative iNSPCs/iSCs are present within post-stroke areas in human brains. Because iNSPCs/iSCs isolated from mouse and human ischemic tissues can differentiate into neuronal lineages in vitro, it is possible that a clearer understanding of iNSPC/iSC profiles and the molecules that regulate iNSPC/iSC fate (e.g., proliferation, differentiation, and survival) would make it possible to perform neural regeneration/repair in patients following stroke. In this article, we introduce the origin and traits of iNSPCs/iSCs based on our reports and recent viewpoints. We also discuss their possible contribution to neurogenesis through endogenous and exogenous iNSPC/iSC therapies following ischemic stroke.