Since astrocyte activation and metabolic function have important roles in regulating neuroinflammation and neuropathology, we examined the serine/threonine kinase LKB1 in astrocytes in a chronic experimental autoimmune encephalomyelitis mouse model of MS. To reduce LKB1, a heterozygous astrocyte-selective conditional knockout (het-cKO) model was used.
Liver kinase B1 (LKB1)/5'-adenosine monophosphate-activated protein kinase (AMPK) signaling, a metabolic checkpoint, plays a neuro-protective role in the pathogenesis of Alzheimer's disease (AD).
Concurrently, loss of LKB1 in DCs enhances their capacity to promote output of regulatory T cells (Tregs) from the thymus, which dominates the outcome of peripheral immune responses, as suggested by increased resistance to asthma and higher susceptibility to cancer in CD11c<sup>ΔLKB1</sup> mice.
STK11 gene mutations may provide insights in the development of multiple cartilaginous tumors in enchondromatosis, this tumor suppressor gene having been shown in animal models to regulate both chondrocyte maturation and growth plate organization during development.
Our data provided new evidence supporting the preventive role of 500 mg/(kg·bw·day) APE treatment in the HFD-induced hepatic steatosis in C57BL/6 mice via the LKB1/AMPK pathway.
Importantly, we further found that mTOR1 inhibitor rapamycin dominantly inhibited <i>in vitro</i> cellular proliferation, while FAK inhibitor PF-573288 drastically decreased invasion of LKB1-attenuated glioblastoma cells.
Myocardial energy metabolism and mitochondria were examined in atrial tissue samples from patients and mice (cardiac-specific LKB1 knock-out) with HF and/or AF.
Myocardial energy metabolism and mitochondria were examined in atrial tissue samples from patients and mice (cardiac-specific LKB1 knock-out) with HF and/or AF.
Here we present an unusual case of a patient with TP53-mutated chronic lymphocytic leukemia (CLL) treated with a PI3Kδ inhibitor evolving to clonally related Langerhans cell histiocytosis (LCH) with acquired BRAF V600E and STK11 mutations and loss of expression of PAX-5 and other examined B cell markers.
Mutations in KRAS, MYC, and PIK3R1 were restricted to WTX-mutated WT, mutations in AKT, CKDN2A, EFGR, HRAS, MET, and RET were restricted to WT without WTX mutation, and mutations in BRAF, CTTNB1, NRAS, PDGFRA, and STK11 were seen in both groups.
Because AMPK phosphorylation is required for kinase activity, we interpret our findings as evidence that indirect AMPK activators are more effective for treating pain hypersensitivity after incision because they can drive increased p-AMPK through upstream kinases like LKB1.
Pregnancy exposure to carbon black nanoparticles exacerbates bleomycin-induced lung fibrosis in offspring via disrupting LKB1-AMPK-ULK1 axis-mediated autophagy.
Whole-exome and Sanger sequencing identified somatic mutations in STK11 (a causative gene of Peutz-Jegher syndrome; n=3), CTNNB1 (n=2), and APC (a gene of familial adenomatous polyposis; n=1) in ICPNs, while those alterations were exceptional in papillary and nonpapillary GBCs.
Although LKB1 has traditionally been considered a tumor suppressor, our data indicates that it may have a complex role in the thyroid gland, where its activation appears to be frequently associated with follicular thyroid carcinoma in both mice and humans.
Our recent study generated an adipocyte-specific Lkb1 and mTOR double knockout (DKO) mouse model and found that DKO of Lkb1 and mTOR caused reduction of brown adipose tissue (BAT) and inguinal white adipose tissue (iWAT) mass but increase of liver mass.
The interactions between RPS6KB1, PTEN, ATM, HSP90AA1, SNRK, PRKAA2, SMARCA4, HSPA1A, and STK11 may play important roles in the abnormal cardiac function of KD.
Importantly, we further found that mTOR1 inhibitor rapamycin dominantly inhibited <i>in vitro</i> cellular proliferation, while FAK inhibitor PF-573288 drastically decreased invasion of LKB1-attenuated glioblastoma cells.