STK11

(redirected from LKB1)

STK11

A gene on chromosome 19p13.3 that encodes a ubiquitously expressed serine/threonine-protein kinase which controls the activity of AMP-activated protein kinase (AMPK) family members, playing a role in various cellular processes such as cell metabolism, cell polarity, apoptosis and DNA damage response. STK11 acts by phosphorylating the T-loop of AMPK family proteins, upregulating their activity.

Molecular pathology
Defects in STK11 are a cause of Peutz-Jeghers syndrome; it has been linked to testicular germ cell tumours and sporadically to non-small cell carcinomas of the lung. Defects in STK11 also promote carcinogenesis, including lung cancer progression and metastasis, and confers in lung adenocarcinoma the ability to trans-differentiate into squamous cell carcinoma.
References in periodicals archive ?
Working in mice, researchers showed how, at the molecular level, loss of LKB1 in regulatory T cells disrupted cell metabolism and function.
Identification of the sucrose non-fermenting related kinase SNRK, as a novel LKB1 substrate.
Transfection with siRNA was used to knock down LKB1, and 2-(N-(7-nitrobenz-2-oxa-1, 3-diazol-4-yl) amino)-2-deoxyglucose (2-NBDG), an effective tracer, was used to detect glucose uptake.
In mammals, the main upstream kinase phosphorylating Thr172 is the liver kinase 1-Ste20Related Adaptor-Mouse protein 25 (LKB1-STRAD-MO25) heterotrimeric complex, a biologically active unit containing the tumour suppressor kinase LKB1 [27, 28].
AMPK is mediated by enzymes such as LKB1, a tumor suppressor, and when AMPK is activated it inhibits anabolic processes and activates catabolic process [5].
It is an established concept that in a fifth of lung cancer cases, an anti-cancer gene called LKB1 (also known as STK11) is absent.
Peutz-Jeghers syndrome is a rare genetic disorder which is associated with mutation of the LKB1 gene on chromosome 19.
Regulation of bile canalicular network formation & maintenance by AMPP-activated protein kinease LKB1.
Several mTOR signaling pathway components such as mTOR, AKT and LKB1 are HSP90 client proteins.
A novel germline mutation of the LKB1 gene in a patient with Peutz-Jeghers syndrome with early-onset gastric cancer.
In some cases, activation of AMPK requires phosphorylation of T-172 by an upstream protein kinase such as LKB1 (Hawley et al.
Nonetheless, more recent experimental evidence has focused on the ability of this biguanide to activate AMPK via the tumor suppressor LKB1 (26), a tumor suppressor kinase whose inactivation leads to Peutz-Jeghers syndrome, a genetic condition characterized by colorectal polyps and predisposition to malignant tumors of various tissues (27).