M. N. Hall

ALK signalling primes the DNA damage response sensitizing ALK-driven neuroblastoma to ATR inhibition

This study identifies ALK signaling's role in enhancing DNA damage response in neuroblastoma, showing that combined ATR/ALK inhibition leads to sustained tumor response and differentiation.

Hepatic mTORC2 compensates for loss of adipose mTORC2 in mediating energy storage and glucose homeostasis

This study shows that loss of adipose mTORC2 leads to increased hepatic lipogenesis and hypertriglyceridemia, but simultaneous inhibition in both tissues causes severe insulin resistance.

Elevated arginine levels in liver tumors promote metabolic reprogramming and tumor growth

The paper shows elevated arginine levels in liver tumors drive metabolic reprogramming and tumor growth through feedback loops involving ASNS and arginase 1.

Adipose mTORC2 is essential for arborization of sensory neurons in white adipose tissue and whole-body energy homeostasis

The paper identifies adipose mTORC2's role in sensory neuron arborization in white adipose tissue and links it to systemic insulin resistance.

Proteogenomic characterization of hepatocellular carcinoma

This study identifies differentially regulated pathways and candidate driver genes in hepatocellular carcinomas through proteogenomic analysis across clinical stages and etiologies.

Colitis is associated with loss of LHPP and up-regulation of histidine phosphorylation in intestinal epithelial cells

The paper shows that intestinal inflammation correlates with loss of LHPP and increased histidine phosphorylation in IECs, but LHPP loss alone does not cause inflammation.

The 3.2A resolution structure of human mTORC2

This study presents a 3.2 Å resolution cryo-EM structure of human mTORC2, revealing structural features and regulatory mechanisms.

Diet-induced loss of adipose Hexokinase 2 triggers hyperglycemia

The paper shows that loss of Hexokinase 2 in adipose tissue due to high fat diet leads to hyperglycemia through systemic glucose homeostasis disruption.

mTOR dependent transformed human cells have a distinct set of essential genes from bcr-abl transformed cells

The paper identifies essential genes for mTOR-dependent cancer growth that are not essential for bcr-abl transformed cells, suggesting distinct therapeutic targets.