Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P17931 (
galectin-3
)
2,860
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Increased mTORC1 signaling from
TSC1/TSC2
inactivation is found in cancer and causes tuberous sclerosis complex (TSC). The role of mesenchymal-derived cells in TSC tumorigenesis was investigated through disruption of
Tsc2
in craniofacial and limb bud mesenchymal progenitors. Tsc2cKO
Prrx1-cre
mice had shortened lifespans and extensive hamartomas containing abnormal tortuous, dilated vessels prominent in the forelimbs. Abnormalities were blocked by the mTORC1 inhibitor sirolimus. A Tsc2/mTORC1 expression signature identified in Tsc2-deficient fibroblasts was also increased in bladder cancers with
TSC1
/
TSC2
mutations in the TCGA database. Signature component
Lgals3
encoding
galectin-3
was increased in Tsc2-deficient cells and serum of Tsc2cKO
Prrx1
-cre mice.
Galectin-3
was increased in TSC-related skin tumors, angiomyolipomas, and lymphangioleiomyomatosis with serum levels in patients with lymphangioleiomyomatosis correlating with impaired lung function and
angiomyolipoma
presence. Our results demonstrate Tsc2-deficient mesenchymal progenitors cause aberrant morphogenic signals, and identify an expression signature including
Lgals3
relevant for human disease of
TSC1/TSC2
inactivation and mTORC1 hyperactivity.
...
PMID:Tsc2 disruption in mesenchymal progenitors results in tumors with vascular anomalies overexpressing
Lgals3
. 2869 25
