Mgat5;Pten

There is no network for this step.

Fullscreen mode

Hide graph

Legend

Genetic mutants with Mgat5, Pten alterations

Names of genes are ordered alphabetically. For the order of interventions, please see the specific paper.

Lifespan (days)
450.0
Lifespan change (compared to wild type)
-33.33%
Phenotype
Median survival for Mgat5+/- male mice is similar to that of wild-type C57BL6 mice. In contrast, median survival for Pten+/- males was 417, in particular due early cancer development (mainly lymphomas). The survival of Pten+/- is slightly ameliorated in males by the Mgat5+/- mutation.
Lifespan comparisons
Double mutant Mgat5(KO);Pten(KO) has a lifespan of 450.0 days, while single mutant Mgat5(KO) has a lifespan of 675.0 days, single mutant Pten(KO) has a lifespan of 417.0 days and wild type has a lifespan of 675.0 days.
Type of interaction
See methods
Dependent
Citation
View abstract
Cheung P, Dennis JW, 2007, Mgat5 and Pten interact to regulate cell growth and polarity. Glycobiology. 17(7):767-73 17400585 Click here to select all mutants from this PubMed ID in the graph
Abstract
Phosphatase and tensin homolog (Pten) phosphatase opposes intracellular phosphoinositide 3-kinase (PI3K)/Akt signaling and is a potent tumor suppressor, while Golgi beta1,6 N-acetylglucosaminyltransferase V (Mgat5) is positively associated with cancer progression and metastasis. beta1,6GlcNAc-branched N-glycans on receptor glycoproteins promote their surface residency and sensitizes cells to growth factor signaling. Here we demonstrate that the Pten heterozygosity in mouse embryonic fibroblasts enhances cell adhesion-dependent PI3K/Akt signaling, cell spreading, and proliferation, while Pten/Mgat5 double mutant cells are normalized. However, planar asymmetry typical of fibroblasts and invasive carcinomas is not fully rescued, suggesting that Mgat5 and Pten function together to regulate the membrane dynamics of PI3K/Akt signaling typical of motile cells. Pten heterozygosity was associated with increased surface beta1,6GlcNAc-branched N-glycans, suggesting positive feedback from PI3K signaling to N-glycan branching. In vivo, Mgat5(-/-) Pten(+/-) and Mgat5(+/-)Pten(+/-)mutant mice showed a small but significant increase in longevity compared with Pten(+/-) mice. Taken together, our results reveal that Mgat5 and Pten interact in an opposing manner to regulate cellular sensitivities to extracelluar growth cues.

Lifespan (days)
440.0
Lifespan change (compared to wild type)
-34.81%
Phenotype
Median survival for Mgat5-/- male mice is reduced to 520, compared with >650 days for wild-type C57BL6 mice. Median survival for Pten+/- males is reduced even more to 417, in particular due early cancer development (mainly lymphomas). The survival of Pten+/- is slightly ameliorated in males by the Mgat5-/- mutation.
Lifespan comparisons
Double mutant Mgat5(KO);Pten(KO) has a lifespan of 440.0 days, while single mutant Mgat5(KO) has a lifespan of 520.0 days, single mutant Pten(KO) has a lifespan of 417.0 days and wild type has a lifespan of 675.0 days.
Type of interaction
See methods
Dependent
Citation
View abstract
Cheung P, Dennis JW, 2007, Mgat5 and Pten interact to regulate cell growth and polarity. Glycobiology. 17(7):767-73 17400585 Click here to select all mutants from this PubMed ID in the graph
Abstract
Phosphatase and tensin homolog (Pten) phosphatase opposes intracellular phosphoinositide 3-kinase (PI3K)/Akt signaling and is a potent tumor suppressor, while Golgi beta1,6 N-acetylglucosaminyltransferase V (Mgat5) is positively associated with cancer progression and metastasis. beta1,6GlcNAc-branched N-glycans on receptor glycoproteins promote their surface residency and sensitizes cells to growth factor signaling. Here we demonstrate that the Pten heterozygosity in mouse embryonic fibroblasts enhances cell adhesion-dependent PI3K/Akt signaling, cell spreading, and proliferation, while Pten/Mgat5 double mutant cells are normalized. However, planar asymmetry typical of fibroblasts and invasive carcinomas is not fully rescued, suggesting that Mgat5 and Pten function together to regulate the membrane dynamics of PI3K/Akt signaling typical of motile cells. Pten heterozygosity was associated with increased surface beta1,6GlcNAc-branched N-glycans, suggesting positive feedback from PI3K signaling to N-glycan branching. In vivo, Mgat5(-/-) Pten(+/-) and Mgat5(+/-)Pten(+/-)mutant mice showed a small but significant increase in longevity compared with Pten(+/-) mice. Taken together, our results reveal that Mgat5 and Pten interact in an opposing manner to regulate cellular sensitivities to extracelluar growth cues.

Lifespan (days)
310.0
Lifespan change (compared to wild type)
-55.71%
Phenotype
Median survival for Mgat5+/- female mice is slightly reduced to 600 compared to that of >650 in wild-type C57BL6 mice. In contrast, median survival for Pten+/- females is only 289, in particular due early cancer development (mainly lymphomas). The survival of Pten+/- is slightly ameliorated in females by the Mgat5+/- mutation.
Lifespan comparisons
Double mutant Mgat5(KO);Pten(KO) has a lifespan of 310.0 days, while single mutant Mgat5(KO) has a lifespan of 600.0 days, single mutant Pten(KO) has a lifespan of 289.0 days and wild type has a lifespan of 700.0 days.
Type of interaction
See methods
Dependent
Citation
View abstract
Cheung P, Dennis JW, 2007, Mgat5 and Pten interact to regulate cell growth and polarity. Glycobiology. 17(7):767-73 17400585 Click here to select all mutants from this PubMed ID in the graph
Abstract
Phosphatase and tensin homolog (Pten) phosphatase opposes intracellular phosphoinositide 3-kinase (PI3K)/Akt signaling and is a potent tumor suppressor, while Golgi beta1,6 N-acetylglucosaminyltransferase V (Mgat5) is positively associated with cancer progression and metastasis. beta1,6GlcNAc-branched N-glycans on receptor glycoproteins promote their surface residency and sensitizes cells to growth factor signaling. Here we demonstrate that the Pten heterozygosity in mouse embryonic fibroblasts enhances cell adhesion-dependent PI3K/Akt signaling, cell spreading, and proliferation, while Pten/Mgat5 double mutant cells are normalized. However, planar asymmetry typical of fibroblasts and invasive carcinomas is not fully rescued, suggesting that Mgat5 and Pten function together to regulate the membrane dynamics of PI3K/Akt signaling typical of motile cells. Pten heterozygosity was associated with increased surface beta1,6GlcNAc-branched N-glycans, suggesting positive feedback from PI3K signaling to N-glycan branching. In vivo, Mgat5(-/-) Pten(+/-) and Mgat5(+/-)Pten(+/-)mutant mice showed a small but significant increase in longevity compared with Pten(+/-) mice. Taken together, our results reveal that Mgat5 and Pten interact in an opposing manner to regulate cellular sensitivities to extracelluar growth cues.

Lifespan (days)
400.0
Lifespan change (compared to wild type)
-42.86%
Phenotype
Median survival for Mgat5-/- female mice is reduced to 522, compared with >650 days for wild-type C57BL6 mice. Median survival for Pten+/- females is reduced even more to 289, in particular due early cancer development (mainly lymphomas). The survival of Pten+/- is slightly ameliorated in males by the Mgat5-/- mutation.
Lifespan comparisons
Double mutant Mgat5(KO);Pten(KO) has a lifespan of 400.0 days, while single mutant Mgat5(KO) has a lifespan of 522.0 days, single mutant Pten(KO) has a lifespan of 289.0 days and wild type has a lifespan of 700.0 days.
Type of interaction
See methods
Dependent
Citation
View abstract
Cheung P, Dennis JW, 2007, Mgat5 and Pten interact to regulate cell growth and polarity. Glycobiology. 17(7):767-73 17400585 Click here to select all mutants from this PubMed ID in the graph
Abstract
Phosphatase and tensin homolog (Pten) phosphatase opposes intracellular phosphoinositide 3-kinase (PI3K)/Akt signaling and is a potent tumor suppressor, while Golgi beta1,6 N-acetylglucosaminyltransferase V (Mgat5) is positively associated with cancer progression and metastasis. beta1,6GlcNAc-branched N-glycans on receptor glycoproteins promote their surface residency and sensitizes cells to growth factor signaling. Here we demonstrate that the Pten heterozygosity in mouse embryonic fibroblasts enhances cell adhesion-dependent PI3K/Akt signaling, cell spreading, and proliferation, while Pten/Mgat5 double mutant cells are normalized. However, planar asymmetry typical of fibroblasts and invasive carcinomas is not fully rescued, suggesting that Mgat5 and Pten function together to regulate the membrane dynamics of PI3K/Akt signaling typical of motile cells. Pten heterozygosity was associated with increased surface beta1,6GlcNAc-branched N-glycans, suggesting positive feedback from PI3K signaling to N-glycan branching. In vivo, Mgat5(-/-) Pten(+/-) and Mgat5(+/-)Pten(+/-)mutant mice showed a small but significant increase in longevity compared with Pten(+/-) mice. Taken together, our results reveal that Mgat5 and Pten interact in an opposing manner to regulate cellular sensitivities to extracelluar growth cues.

Search genes: Mgat5 Pten

Entrez ID
Symbol
GenAge
MGI ID

107895
Mgat5
View on GenAge (Mgat5)
MGI:894701

mannoside acetylglucosaminyltransferase 5

Entrez ID
Symbol
GenAge
MGI ID

19211
Pten
View on GenAge (Pten)
MGI:109583

phosphatase and tensin homolog

Orthologs of Mgat5;Pten in SynergyAge

Show in SynergyAge
Species	Gene

Not in SynergyAge
Species	Gene

Orthologs of Mgat5 in SynergyAge

Show in SynergyAge
Species	Gene

Not in SynergyAge
Species	Gene
Caenorhabditis elegans	gly-2

Orthologs of Pten in SynergyAge

Show in SynergyAge
Species	Gene

Not in SynergyAge
Species	Gene
Drosophila melanogaster	Pten