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FLASH GENE

Symbol

STK11

contributors: mct/pgu/shn - updated : 14-06-2016

HGNC name	serine/threonine kinase 11
HGNC id	11389

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

ASSOCIATED DISORDERS

corresponding disease(s)

PJS1

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function tumoral somatic mutation       in sporadic testicular cancer, malignant skin melanoma and laryngeal tumor tumoral somatic mutation       in gastrointestinal hamartomatous polyps in PJS1(familial forms) tumoral germinal mutation       in gastrointestinal hamartomatous polyps in PJS1(familial forms) tumoral   LOH     in PJS1 with polyposis resistant to transformation tumoral somatic mutation       in lung adenocarcinomas tumoral       loss of function in ovarian, intestinal and pancreatic cancer tumoral germinal mutation       in head and neck squamous cell carcinoma tumoral     --low   in breast cancer tumoral     --over   in breast cancer cells resulted in significant inhibition of invasion and significantly associated with a decrease in microvessel density tumoral somatic mutation       and homozygous inactivating mutations in non-small-cell lung cancers tumoral   LOH     in &8764;30p100 of lung adenocarcinomas, contribute significantly to lung cancer malignancy progression ( tumoral   deletion     frequent homozygous deletion in non-small cell lung cancer

Susceptibility

to malignancies, to pancreatic cancer to absence of ovulatory response to treatment with metformin in polycystic ovary syndrome (PCOS)

Variant & Polymorphism SNP , other	C allele of a single nucleotide polymorphism associated with a significantly decreased chance of ovulation in PCOS women treated with metformin

Candidate gene
Marker
Therapy target
	System Type Disorder Pubmed cancer digestive colon COX-2 as a potential target for chemoprevention in Peutz-Jeghers polyposis patients

ANIMAL & CELL MODELS

	mice with a targeted disruption of Lkb1 die at midgestation, with the embryos showing neural tube defects, mesenchymal cell death and deregulation of vascular endothelial growth factor (VEGF) expression
	Lkb1 (+/-) mice develop hamartomatous polyps in the glandular stomach
	Lkb1(-/-) mice died in utero between 8.5 and 9.5 days postcoitum with developmental retardation and multiple gastric adenomatous polyps
	in somatically activatable mutant Kras- driven model of mouse lung cancer, pulmonary tumorigenesis was accelerated by hemizygous inactivation of Lkb1 (STK11)
	LKB1-deficient murine embryonic fibroblasts show nearly complete loss of Thr-172 phosphorylation and downstream AMPK signaling in response to a variety of stimuli that activate AMPK (
	deletion of LKB1 in liver of adult mice result in a loss of AMPK activityand hyperglycemia with increased gluconeogenic and lipogenic gene expression
	LKB1-KO mice displayed biatrial enlargement with atrial fibrillation and cardiac dysfunction at 4 weeks of age
	deletion of Stk11 gene in mice caused increased haematopoietic stem cell (HSC) division, rapid HSC depletion and pancytopenia (
	Lkb1-deficient haematopoietic stem cell have reduced mitochondrial membrane potential and ATP levels, exhibit defects in centrosomes and mitotic spindles in culture, and become aneuploid (
	Lkb1 inactivation in adult mice causes loss of haematopoietic stem cell quiescence followed by rapid depletion of all haematopoietic subpopulations (
	Lkb1-deficient bone marrow cells exhibit mitochondrial defects, alterations in lipid and nucleotide metabolism, and depletion of cellular ATP (
	ablation of Lkb1 in adult mice results in severe pancytopenia and subsequent lethality (