Heterozygous inactivation of tsc2 enhances tumorigenesis in p53 mutant zebrafish
SUMMARY Tuberous sclerosis complex (TSC) is a multi-organ disorder caused by mutations of the TSC1 or TSC2 genes. A key function of these genes is to inhibit mTORC1 (mechanistic target of rapamycin complex 1) kinase signaling. Cells deficient for TSC1 or TSC2 have increased mTORC1 signaling and give...
Main Authors: | Seok-Hyung Kim, Marie L. Kowalski, Robert P. Carson, L. Richard Bridges, Kevin C. Ess |
---|---|
Format: | Article |
Language: | English |
Published: |
The Company of Biologists
2013-07-01
|
Series: | Disease Models & Mechanisms |
Online Access: | http://dmm.biologists.org/content/6/4/925 |
Similar Items
-
Non-canonical functions of a mutant TSC2 protein in mitotic division.
by: Mary-Bronwen L Chalkley, et al.
Published: (2023-01-01) -
Neuronal and glia abnormalities in Tsc1-deficient forebrain and partial rescue by rapamycin
by: Robert P. Carson, et al.
Published: (2012-01-01) -
BRCA2 and TP53 collaborate in tumorigenesis in zebrafish.
by: Heather R Shive, et al.
Published: (2014-01-01) -
Zebrafish model of tuberous sclerosis complex reveals cell-autonomous and non-cell-autonomous functions of mutant tuberin
by: Seok-Hyung Kim, et al.
Published: (2011-03-01) -
mTOR-related neuropathology in mutant tsc2 zebrafish: Phenotypic, transcriptomic and pharmacological analysis
by: Chloë Scheldeman, et al.
Published: (2017-12-01)