| |||
| |||
|
      |
|
 |
|
| |||||||||||
| |||||||||||
| |||||||||||
| | | | ||||||||
| In brief: January 2002Mouse Models
Analysis of lung tumor initiation and progression using conditional expression of oncogenic K-ras.
Induction and apoptotic regression of lung adenocarcinomas by regulation of a K-Ras transgene in the presence and absence of tumor suppressor genes.
Oncogenic KRAS mutations can give rise to lung adenocarcinomas, but where do these tumours arise, and is KRAS also important for tumour maintenance? Two new mouse models address these questions. Jackson and colleagues can switch on oncogenic Kras in a few cells by administering a vector encoding an enzyme that edits a stop codon out of an engineered KRas gene. This has allowed them to identify a progenitor-like cell as the cell of origin for lung adenocarcinoma. Fisher and colleagues can switch Kras on and off at will. In this model, tumours regress rapidly by apoptosis when Kras expression is switched off, even in the absence of p53, Ink4a or Arf. This has implications for therapy as it indicates that blocking the RAS pathway, even in advanced tumours, could lead to apoptosis of tumour cells. G-Protein-Coupled Receptors
Constitutive activity of histamine H3 receptors stably expressed in SK-N-MC cells: display of agonism and inverse agonism by H3 antagonists.
Over the past decade, it has become clear that many G-protein-coupled receptors can be active in the absence of an endogenous agonist, a phenomenon known as constitutive activity. This has led to the reclassification of many antagonists as 'inverse agonists'. The histamine H3 receptor, a potential drug target for the regulation of neural activity, is now observed to show agonist-independent signalling, and classical H3 receptor 'antagonists' are shown to be regulators of constitutive activity. | | |||||||||
| |||||||||||
 | |||||||||||
| |||||||||||
| |||||||||||
| |||||||||||
HOME | SIGNALING UPDATE | MOLECULE PAGES | DATA CENTER | ABOUT US | |||||||||||
| |||||||||||
