Differential modulation of C. elegans motor behavior by NALCN and two-pore domain potassium channels.

Two-pore domain potassium channels (K2P) are a large family of "background" channels that allow outward "leak" of potassium ions. The NALCN/UNC80/UNC79 complex is a non-selective channel that allows inward flow of sodium and other cations. It is unclear how K2Ps and NALCN differentially modulate animal behavior.

The NALCN Channel Regulator UNC-80 Functions in a Subset of Interneurons To Regulate Reversal Behavior.

NALCN (eak hannel, on-selective) is a conserved, voltage-insensitive cation channel that regulates resting membrane potential and neuronal excitability. UNC79 and UNC80 are key regulators of the channel function. However, the behavioral effects of the channel complex are not entirely clear and the neurons in which the channel functions remain to be identified.

Defective Expression of Mitochondrial, Vacuolar H-ATPase and Histone Genes in a Model of SMA.

Spinal muscular atrophy (SMA) is a severe motor neuron degenerative disease caused by loss-of-function mutations in the survival motor neuron gene . It is widely posited that defective gene expression underlies SMA. However, the identities of these affected genes remain to be elucidated.

RBM-5 modulates U2AF large subunit-dependent alternative splicing in C. elegans.

A key step in pre-mRNA splicing is the recognition of 3' splicing sites by the U2AF large and small subunits, a process regulated by numerous trans-acting splicing factors. How these trans-acting factors interact with U2AF in vivo is unclear. From a screen for suppressors of the temperature-sensitive (ts) lethality of the C.

Identification of ANKDD1B variants in an ankylosing spondylitis pedigree and a sporadic patient.

Background: Ankylosing spondylitis (AS) is a debilitating autoimmune disease affecting tens of millions of people in the world. The genetics of AS is unclear. Analysis of rare AS pedigrees might facilitate our understanding of AS pathogenesis.