LKB1 loss of function studied in vivo

Abstract

a b s t r a c tRecent developments have placed the serine/threonine kinase LKB1 on the crossroads linking energy metabolism, cell structure and cancer progression and that its deletion can affect tumorigenesis, metastasis, cell adhesion and polarity. LKB1 can regulate a host of different functions which all have potential to impact upon the initiation and progression of neoplastic disease. To understand the phenotypic consequences of LKB1 loss in a range of different settings, a number of animal models of loss of function have been generated and analyzed. In this review we summarize recent data generated from a range of these models, which reveal clear tissue specific differences in LKB1 function in vivo and in the consequences of its loss.

Metabolic regulator LKB1 is crucial for Schwann cell–mediated axon maintenance

“…Some notable exceptions included the down-regulation of Lgi1, and the up-regulation of chemokine ligands 4/14, and interleukin 10 receptor α, respectively. Curiously, but compatible with reported LKB1 deletion phenotypes 29 , transcripts involved in melanin biosynthesis (e.g. premelanosome protein Pme1, tyrosinase-related protein 1) were strongly up-regulated in LKB1 depleted nerves.…”

The regulation and function of the NUAK family

“…Overall, as illustrated in Fig. 1, different ARKs might share similar regulatory roles in the regulation of cellular physiology such as cell polarity and cell motility (Shorning & Clarke 2011). More investigations of interplays between AMPK and its associated kinases would be required to further elucidate collaborative roles of different AMPK kinases.…”

Association between STK11 Gene Polymorphisms and Coronary Artery Disease in Type 2 Diabetes in Han Population in China

“…The mechanism could be explained that the endothelial cells were relying on TGF β -based communication between endothelium and smooth muscles to recruit smooth muscle cells into the newly formed blood vessels. And the role of STK11 in this process appeared to regulate TGF β availability to the nearby smooth muscle and mesenchymal cells [7]. Taken together, changes in the expression of STK11 gene or, in other words, in its functions may affect cardiac and vascular endothelial function.…”

“…It was initially discovered because of its role as a tumor suppressor and mutated in a number of cancers (Peutz-Jeghers Syndrome, lung and cervical cancer) [7]. But it is becoming clear that STK11 has a wide range of biological roles that reach far beyond that.…”