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The ATM inhibitor KU-55933 bound to the ATM kinase domain is shown next to an HIV-1-infected T cell. Cover designed with the help of Lotte Mai Lessware and Xiao-Ling Cockcroft (T-cell image copyright J.L. Carson/Custom Medical Stock Photo).
Talin is a core component of the integrin adhesion complex. It is now shown that talin also regulates transcription, an activity that is apparently independent of its interaction with integrins. Talin represses the expression of Drosophila melanogaster DE-cadherin through an unknown molecular mechanism.
Conditional knockout of the KAP3 subunit from the kinesin motor KIF3 alters tissue patterning and causes abnormal proliferation of neural progenitor cells in the mouse brain. Impaired transport of N-cadherin to the surface of these cells may be one explanation for how such defects arise.
Vesicle formation at the trans-Golgi network may be mechanistically more similar to endocytic vesicle formation at the plasma membrane than previously thought. Both processes share common components including the dynamin-binding protein cortactin.
By what molecular mechanisms do microtubules regulate the spatial distribution of actin assembly in cells? In fission yeast, a novel SH3-domain-containing protein, Tea4p, acts to bridge the microtubule plus-end-binding protein Tea1p with the actin-nucleating formin protein For3p.
The HIV type 1 (HIV-1) life-cycle involves a number of cellular cofactors. Some are essential for HIV-1 replication and thus may serve as targets for therapeutic intervention. An emerging role for cellular DNA repair in HIV-1 infection suggests that inhibition of these repair functions may lead to suppression of viral replication.
Phosphorylation of synaptojanin 1 by the EphB2 receptor tyrosine kinase is a molecular switch. This phosphorylation prevents the interaction of synaptojanin 1 with endophilin and promotes endocytosis. Subsequent dephosphorylation initiates an interaction with endophilin, leading to clathrin uncoating and fusion with endosomes.
Highly localized Ca2+ signals called Ca2+ sparks have been widely reported in all mammalian muscle types except adult skeletal muscle. We now learn that these mysteriously absent sparks can be seen during stress or disease, raising the question of how these signals become unmasked in these conditions.