EMBO Reports
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FIP200 regulates targeting of Atg16L1 to the isolation membrane Autophagosome formation is a dynamic process that is strictly controlled by autophagy‐related (Atg) proteins. However, how these Atg proteins are recruited to the autophagosome formation site or autophagic membranes remains poorly understood. Here, we found that FIP200, which is involved in proximal events, directly interacts with Atg16L1, one of the downstream Atg factors, in an Atg14‐ and phosphatidylinositol 3‐kinase‐independent manner. Atg16L1 deletion mutants, which lack the FIP200‐interacting domain, are defective in proper membrane targeting. Thus, FIP200 regulates not only early events but also late events of autophagosome formation through direct interaction with Atg16L1.
EMBO Reports - Tập 14 Số 3 - Trang 284-291 - 2013
Hrr25 kinase promotes selective autophagy by phosphorylating the cargo receptor <scp>A</scp> tg19
EMBO Reports - Tập 15 Số 8 - Trang 862-870 - 2014
Sex and gender differences in health The new concept of evidence‐based sex and gender medicine—which includes the fundamental differences of biology and behaviour between women and men—should improve health care for both sexes.
EMBO Reports - Tập 13 Số 7 - Trang 596-603 - 2012
The neurobiology of overeating Is overeating a neurological disorder like drug or alcohol addiction? Recent advances in neuroscience suggest it might be, which could have profound consequences for the treatment of obese people and public health policies to address the growing epidemic of obesity.
EMBO Reports - Tập 13 Số 9 - Trang 785-790 - 2012
Calcium: a fundamental regulator of intracellular membrane fusion?
EMBO Reports - Tập 8 Số 3 - Trang 236-240 - 2007
ChAM, a novel motif that mediates PALB2 intrinsic chromatin binding and facilitates DNA repair The partner and localizer of breast cancer 2 susceptibility protein (PALB2) is crucial for the repair of DNA damage by homologous recombination. Here, we report that chromatin‐association motif (ChAM), an evolutionarily conserved motif in PALB2, is necessary and sufficient to mediate its chromatin association in both unperturbed and damaged cells. ChAM is distinct from the previously described PALB2 DNA‐binding regions. Deletion of ChAM decreases PALB2 and Rad51 accumulation at DNA damage sites and confers cellular hypersensitivity to the genotoxic drug mitomycin C. These results suggest that PALB2 chromatin association via ChAM facilitates PALB2 function in the cellular resistance to DNA damage.
EMBO Reports - Tập 13 Số 2 - Trang 135-141 - 2012
Structural basis for recruitment of BRCA2 by PALB2 The breast cancer 2, early onset protein (BRCA2) is central to the repair of DNA damage by homologous recombination. BRCA2 recruits the recombinase RAD51 to sites of damage, regulates its assembly into nucleoprotein filaments and thereby promotes homologous recombination. Localization of BRCA2 to nuclear foci requires its association with the partner and localizer of BRCA2 (PALB2), mutations in which are associated with cancer predisposition, as well as subtype N of Fanconi anaemia. We have determined the structure of the PALB2 carboxy‐terminal β‐propeller domain in complex with a BRCA2 peptide. The structure shows the molecular determinants of this important protein–protein interaction and explains the effects of both cancer‐associated truncating mutants in PALB2 and missense mutations in the amino‐terminal region of BRCA2.
EMBO Reports - Tập 10 Số 9 - Trang 990-996 - 2009
Tramtrack69 interacts with the dMi‐2 subunit of the <i>Drosophila</i> NuRD chromatin remodelling complex dMi‐2, the ATPase subunit of the Drosophila nucleosome remodelling and histone deacetylation (dNuRD) complex, was identified in a two‐hybrid screen as an interacting partner of the transcriptional repressor, Tramtrack69 (Ttk69). A short region of Ttk69 is sufficient to mediate this interaction. Ttk69, but not the Ttk88 isoform, co‐purifies with the dNuRD complex isolated from embryo extracts. dMi‐2 and Ttk69 co‐immunoprecipitate from embryonic extracts, indicating that they can associate in vivo . Both dMi‐2 and Ttk69 co‐localize at a number of discrete sites on polytene chromosomes, showing that they bind common target loci. We also demonstrate that dMi‐2 and Ttk interact genetically, indicating a functional interaction in vivo . We propose that Ttk69 represses some target genes by remodelling chromatin structure through the recruitment of the dNuRD complex.
EMBO Reports - Tập 2 Số 12 - Trang 1089-1094 - 2001
Cdc48 and Ufd3, new partners of the ubiquitin protease Ubp3, are required for ribophagy Ubiquitin‐dependent processes can be antagonized by substrate‐specific deubiquitination enzymes involved in many cellular functions. In this study, we show that the yeast Ubp3–Bre5 deubiquitination complex interacts with both the chaperone‐like Cdc48, a major actor of the ubiquitin and proteasome system, and Ufd3, a ubiquitin‐binding cofactor of Cdc48. We observed that these partners are required for the Ubp3–Bre5‐dependent and starvation‐induced selective degradation of yeast mature ribosomes, also called ribophagy. By contrast, proteasome‐dependent degradation does not participate in this process. Our data favour the idea that these factors cooperate to recognize and deubiquitinate specific substrates of ribophagy before their vacuolar degradation.
EMBO Reports - Tập 11 Số 7 - Trang 548-554 - 2010
The ZEB/miR‐200 feedback loop—a motor of cellular plasticity in development and cancer? Epithelial‐to‐mesenchymal transition (EMT) is a fundamental process in development and disease. Zinc‐finger enhancer binding (ZEB) transcription factors (ZEB1 and ZEB2) are crucial EMT activators, whereas members of the miR‐200 family induce epithelial differentiation. They are reciprocally linked in a feedback loop, each strictly controlling the expression of the other. Now data show that EMT not only confers cellular motility, but also induces stem‐cell properties and prevents apoptosis and senescence. Thus the balanced expression of ZEB factors and miR‐200 controls all these processes. We therefore propose that the ZEB/miR‐200 feedback loop is the molecular motor of cellular plasticity in development and disease, and in particular is a driving force for cancer progression towards metastasis by controlling the state of cancer stem cells.
EMBO Reports - Tập 11 Số 9 - Trang 670-677 - 2010
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