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    Gerbe et al. defi ne tuft cells as a new secretory lineage in the intestine. These rare cells can be distinguished from the four other main cell types of the intestinal epithelium by their co-expression of SOX9 (red) and COX1 (green). Microtubules are shown in white. Image courtesy of François Gerbe.
    See page 767.

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ISSN 0021-9525
EISSN 1540-8140
In this Issue

In This Issue

In Focus

Parkinson's disease may be caused by microtubule, rather than mitochondrial complex I, dysfunction.

People & Ideas

Steitz has spent her career uncovering RNA's different cellular avocations.



Rad54’s ATPase activity does not affect accumulation of homologous recombination proteins in repair foci, but influences its dissociation and that of Rad51.

Mesp1, the earliest marker of cardiovascular development in vivo, is used to isolate and characterize multipotent cardiovascular progenitors during ESC differentiation.

Tuft cells represent a fourth type of intestinal secretory cell that constitutes the primary source of endogenous intestinal opioids and are the only epithelial cell that constitutively express cyclooxygenases.

Tdrd5-deficient mice develop a functional haploid genome despite spermiogenesis arrest at the round spermatid stage.

α6β1-integrin interacts with hnRNP-K, an mRNA-binding protein, during oligodendrocyte differentiation to promote translation of MBP mRNA and myelin synthesis.

Phosphorylation of Kvβ2 releases Kv1 channels from microtubules to control their specific distribution at the axonal membrane.

Autocatalytic processing of the Hedgehog ligand from its precursor protein relies on protein disulfide isomerase and ER-associated degradation.

The GAP activity of OATL1, which is recruited to autophagosomes by Atg8, regulates autophagosome–lysosome fusion.

Nup133 links CENP-F, NudE/EL, and the dynein/dynactin complex to anchor centrosomes to the nuclear membrane.

The combination of microtubule depolymerization and the accumulation of cytosolic dopamine and reactive oxygen species selectively affects survival of dopaminergic neurons.

Loss of kindlin-3 impairs activation of β1, β2, and β3 integrin classes, resulting in osteopetrotic defects in osteoclast adhesion and spreading.


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