10 Exons spanning 23 kb, the 10th exon occurs within the 3 untranslated region of the gene. The gene is transcribed in telomere to centromere direction.

The length of this transcript has not been reconciled. The curated human Vega transcript is the longest transcript reported to date (3,627 bp, Vega external transcript). The GeneBank sequence is the same but is shorter (3,286 bp) at the 3 end (NM_000455.4). The exon/intron structures in GeneBank are given for 2 alternative assemblies (aligned with NT_011255.14 and NW_927173.1), of which the NT_0112255.14 is consistent with the Vega annotation. Alternative transcripts although shown to occur, have not be been well characterized.

433 amino acids, 48.6 kDa; N-term with a nuclear localization domain and a putative cytoplasmic retention signal, a kinase domain, and a C-terminal CAAX box prenylation motif.

Ubiquitous, especially high expression in the testis and fetal liver.

Found in both the nucleus and the cytoplasm. Localization is thought to be dependent on interaction with proteins such as BRG1, LIP1, STRAD, MO25.

A serine/threonine protein kinase, recently classified as a part of the Ca2+/ calmodulin kinase group of kinases. STK11 was shown to associate and activate the pseudokinase, STRAD, resulting in the reorganization of non-polarized cells so they form asymmetrical apical and basal structures. Another mechanism by which this may occur is by the interaction of STK11 with the PAR1 family of serine/threonine kinases. AMPK is a protein kinase cascade that plays an important role in regulating energy homeostasis. The first report of an upstream regulator came when it was discovered that STK11, in complex with STRAD and the scaffolding protein MO25, can phosphorylate and activate AMPK. Subsequently, it was demonstrated that STK11 can phosphorylate the T-loop of 12 other AMPK related human kinases. In addition it has been implicated in a range of processes including, chromatin remodeling, cell cycle arrest, ras-induced cell transformation, p53-mediated apoptosis and Wnt signaling.

Orthologs found in several species and include:
Xenopus laevis egg and embryonic kinase 1(XEEK1),
Caenorhabditis elegans partitioning defective gene 4 (PAR4),
mouse LKB1
and drosophila LKB1.

Most mutations identified to date are in the catalytic domain of STK11, indicating that kinase activity is likely essential for its function as a tumor suppressor. Several types of mutations including insertions, deletions, nonsense, missense and splice site alterations have been identified to date. One family has been identified with complete germline deletion of this gene.

Many of the polyps that develop in Peutz-Jeghers syndrome (see below) show loss of heterozygosity and sometimes somatic mutations. Somatic mutations rarely occur in sporadic tumours, with the exception of adenocarcinoma of the lung. The inactivation of the LKB1 can also occur through promoter hypermethylation.