Distinct ubiquitin-ligase complexes define convergent pathways for the degradation of ER proteins.

By Pedro Carvalho, V. Goder, Tom A. Rapoport. Cell, 2006

774 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/57ab74a9fb6e69d61e383f5530d625323012855e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. Tiziana Anelli
2. Annamaria Ruggiano
3. O. Foresti
4. Pedro Carvalho
5. M. Molinari
6. Roberto Sitia
7. D. Hebert

In Molecular Biology

1. Annamaria Ruggiano
2. O. Foresti
3. Pedro Carvalho
4. M. Molinari
5. Roberto Sitia
6. D. Hebert
7. Tiziana Anelli

In Physiology

1. Annamaria Ruggiano
2. O. Foresti
3. Pedro Carvalho

Citations in the corpus

• Protein quality control in the early secretory pathway (2008, background): “Experiments in yeast and mammalian cells have recently shown that molecules involved in ERAD form multiprotein complexes specialized in the handling of topological classes of proteins (Vashist and Ng, 2004; Lilley and Ploegh, 2005; Carvalho et al, 2006).”
• Quality control: ER-associated degradation: protein quality control and beyond. (2014, positive): “For example, OS-9 and XTP3-B, the mammalian homologues of Yos9, use their glycan-binding domain not only to interact with glycans in the misfolded protein but also with Sel1, the mammalian version of Hrd3, which is itself a glycoprotein (Christianson et al., 2008).”
• In and out of the ER: protein folding, quality control, degradation, and related human diseases. (2007, background): “Also, the specific machineries involved in the detection of structural protein defects [the ERAD-L (or Hrd1p complex) to inspect luminal defects, the ERAD-C (or Doa10p complex) for cytosolic ones, and the ERAD-M for structural defects in the transmembrane regions of newly synthesized polypeptides] h”
• Elements of the ERAD ubiquitin ligase Doa10 regulating sequential poly-ubiquitylation of its targets (2022, neutral): “…targeting elements (‘‘degrons’’) in the cytoplasm/nucleoplasm (ERAD-C) (Huyer et al., 2004;Metzger et al., 2008; Ravid et al., 2006) whereas Hrd1 recognizes ERAD substrates with degrons in the ER lumen (ERAD-L) or ER membrane (ERAD-M) (Carvalho et al., 2006; Gauss et al., 2006; Sato et al., 2009).”