JAK-ing up the Response to KIT Inhibition

T cells JAK up integrin activity

Senescent cells have a case of the SADS C ells unravel their centro-meres as they enter senes-cence, Swanson et al. reveal. Senescent cells are metabolically active but no longer capable of dividing. This permanent exit from the cell cycle can be induced by the telomere shortening associated with aging or by other stresses such as the expression of active onco-genes. Despite the importance of s...

The Response of Ventral Tegmental Area Dopaminergic Neurons to Bupropion: Excitation or Inhibition?

Introduction: Antidepressants can modulate brain monoamines by acting on pre-synaptic and postsynaptic receptors. Autoreceptors can reduce the monoamines effect on the somatodendritic or pre-synaptic regions despite its postsynaptic counter effects. The direct effect of some antidepressants is related to its temporal and spatial bioavailability in the vicinity of these receptors (still a matter...

Ang-1: Tie-ing up endothelial adhesion?

"Patch"ing up our tumor signaling knowledge.

The tumor suppressor Patched1 (Ptch1) possesses well-described roles in regulating sonic hedgehog (SHH) signaling in the skin and preventing the formation of basal cell carcinomas (BCCs). In this issue, Kang et al. extend their previous work to show that a naturally occurring allele of Ptch1 found in FVB mice promotes early squamous cell carcinoma (SCC) growth without aberrant activation of the...

NK cell modulation by JAK inhibition

NK cells are innate immune effector cells recognizing and killing virus-infected or malignant cells [1].NK cell function is tightly regulated by a complex balance between various activating and inhibitory NK cell receptors. In addition, several cytokines (IL-2, IL-12, IL-15 and IL-18) mediated via the JAK/STAT pathway are critical for NK cell development and activation. Thus it is tempting to s...