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 ?
LKB1 and AMP-activated protein kinase control of mTOR signalling and growth.
Some oncogenes in lung cancers (alteration in TP53, K EGFR, RAS, CDKN2, FHIT, MYC, LKB1 and RB genes) are shown to affect tumor microenvironment to promote immune escape (14).
Bu sistemle olusturulan bir diger oldukca favori olan model ise Lkb1:LSLK-RasG12D' dir ve insan metastazina oldukca benzer adenokarsinomlar ve skuamoz hucre karsinomlari gelisir (52).
Loss of Lkb1 and Pten leads to lung squamous cell carcinoma with elevated PD-L1 expression.
The LKB1 tumor suppressor negatively regulates mTOR signaling.
The cause of PJS is a mutant gene named STK1, also known as LKB1. This gene is localized at 19p34-p36 and is a serine/threonine kinase that controls growth regulation.
Both these molecules affect similar biological process and it has also been discovered that Sirt1 phosphorylates LKB1, the upstream kinase of AMPK and AMPK activated Sirt1 though Nampt (Cetrullo et al., 2015) AMPK is a serine threonine kinase which acts as a metabolic fuel gauge.
Studies have shown that NUCB2/Nesfatin-1 can promote colon cancer cell migration, invasion, and epithelial-mesenchymal transition through LKB1, AMPK/TORC1/ZEB pathways.[17] A study by Yoo et al.
AMPK promotes its phosphorylation [24] at the Thr172 residue in its a subunit [25] by using an upstream kinase that was identified as a complex between tumor suppressor protein LKB1 and two accessory subunits STRAD and MO25 [26].
AMP competes with ATP for binding to the y regulatory subunit of AMPK [177, 178] and by doing so, greatly increases AMPK activity, but only in the presence of an upstream kinase such as liver kinase B1 (LKB1) [179].
Vasquez et al., "Medicine: the kinase LKB1 mediates glucose homeostasis in liver and therapeutic effects of metformin," Science, vol.