ArticleMolecular and cellular biology2011
Derlin-2-deficient mice reveal an essential role for protein dislocation in chondrocytes.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- Holding Out for a Model: Rhomboid Superfamily in Vertebrate Development and Disease.Journal of cellular physiology · 2025Review
- SEL1L-HRD1-mediated ERAD in mammals.Nature cell biology · 2025Review
- Sex-related differences and associated transcriptional signatures in the brain ventricular system and cerebrospinal fluid development in full-term neonates.Biology of sex differences · 2025Article
- The Derlin-1-Stat5b axis maintains homeostasis of adult hippocampal neurogenesis.EMBO reports · 2024Article
- DERL2 (derlin 2) stabilizes BAG6 (BAG cochaperone 6) in chemotherapy resistance of cholangiocarcinoma.Journal of physiology and biochemistry · 2024Article
- Hypomorphic variants of SEL1L-HRD1 ER-associated degradation are associated with neurodevelopmental disorders.The Journal of clinical investigation · 2024Article
- Deep mutational scanning highlights a role for cytosolic regions in Hrd1 function.Cell reports · 2023Article
- The Role of the Rhomboid Superfamily in ER Protein Quality Control: From Mechanisms and Functions to Diseases.Cold Spring Harbor perspectives in biology · 2023Review
- Mutations in SCNM1 cause orofaciodigital syndrome due to minor intron splicing defects affecting primary cilia.American journal of human genetics · 2022Article
- Integrated profiling of endoplasmic reticulum stress-related DERL3 in the prognostic and immune features of lung adenocarcinoma.Frontiers in immunology · 2022Article
- ERAD components Derlin-1 and Derlin-2 are essential for postnatal brain development and motor function.iScience · 2021Article
- How Is the Fidelity of Proteins Ensured in Terms of Both Quality and Quantity at the Endoplasmic Reticulum? Mechanistic Insights into E3 Ubiquitin Ligases.International journal of molecular sciences · 2021Review
- The role of rhomboid superfamily members in protein homeostasis: Mechanistic insight and physiological implications.Biochimica et biophysica acta. Molecular cell research · 2020Review
- ER-associated degradation in health and disease - from substrate to organism.Journal of cell science · 2019Review
- Schwann cells ER-associated degradation contributes to myelin maintenance in adult nerves and limits demyelination in CMT1B mice.PLoS genetics · 2019Article
- 4-Phenylbutyric Acid Reduces Endoplasmic Reticulum Stress in Chondrocytes That Is Caused by Loss of the Protein Disulfide Isomerase ERp57.Oxidative medicine and cellular longevity · 2019Article
- Quality Control in the Endoplasmic Reticulum: Crosstalk between ERAD and UPR pathways.Trends in biochemical sciences · 2018Review
- Different Forms of ER Stress in Chondrocytes Result in Short Stature Disorders and Degenerative Cartilage Diseases: New Insights by Cartilage-Specific ERp57 Knockout Mice.Oxidative medicine and cellular longevity · 2018Review
- Posttranscriptional Regulation of Glycoprotein Quality Control in the Endoplasmic Reticulum Is Controlled by the E2 Ub-Conjugating Enzyme UBC6e.Molecular cell · 2016Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Protein quality control is a balance between chaperone-assisted folding and removal of misfolded proteins from the endoplasmic reticulum (ER). Cell-based assays have been used to identify key players of the dislocation machinery, including members of the Derlin family. We generated conditional knockout mice to examine the in vivo role of Derlin-2, a component that nucleates cellular dislocation machinery. In most Derlin-2-deficient tissues, we found constitutive upregulation of ER chaperones and IRE-1-mediated induction of the unfolded protein response. The IRE-1/XBP-1 pathway is required for development of highly secretory cells, particularly plasma cells and hepatocytes. However, B lymphocyte development and antibody secretion were normal in the absence of Derlin-2. Likewise, hepatocyte function was unaffected by liver-specific deletion of Derlin-2. Whole-body deletion of Derlin-2 results in perinatal death. The few mice that survived to adulthood all developed skeletal dysplasia, likely caused by defects in collagen matrix protein secretion by costal chondrocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.