ArticleMolecular biology of the cell2015
Sil1, a nucleotide exchange factor for BiP, is not required for antibody assembly or secretion.
Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Sil1-deficient fibroblasts generate an aberrant extracellular matrix leading to tendon disorganisation in Marinesco-Sjögren syndrome.Journal of translational medicine · 2024Article
- Role of the HSP70 Co-Chaperone SIL1 in Health and Disease.International journal of molecular sciences · 2021Review
- Intracellular Lipid Accumulation and Mitochondrial Dysfunction Accompanies Endoplasmic Reticulum Stress Caused by Loss of the Co-chaperoneFrontiers in cell and developmental biology · 2021Article
- Development and Initial Characterization of Cellular Models for COG Complex-Related CDG-II Diseases.Frontiers in genetics · 2021Article
- Early Emergence of Adaptive Mechanisms Sustaining Ig Production: Application to Antibody Therapy.Frontiers in immunology · 2021Review
- Functional Role of SIL1 in Neurodevelopment and Learning.Neural plasticity · 2019Article
- SIL1, the endoplasmic-reticulum-localized BiP co-chaperone, plays a crucial role in maintaining skeletal muscle proteostasis and physiology.Disease models & mechanisms · 2018Article
- SIL1 functions as an oncogene in glioma by AKT/mTOR signaling pathway.OncoTargets and therapy · 2018Article
- In-depth phenotyping of lymphoblastoid cells suggests selective cellular vulnerability in Marinesco-Sjögren syndrome.Oncotarget · 2017Article
- The Role of BiP Retrieval by the KDEL Receptor in the Early Secretory Pathway and its Effect on Protein Quality Control and Neurodegeneration.Frontiers in molecular neuroscience · 2017Review
- Sil1-Mutant Mice Elucidate Chaperone Function in Neurological Disorders.Journal of neuromuscular diseases · 2016Article
- BiP and its nucleotide exchange factors Grp170 and Sil1: mechanisms of action and biological functions.Journal of molecular biology · 2015Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Sil1 is a nucleotide exchange factor for the endoplasmic reticulum chaperone BiP, and mutations in this gene lead to Marinesco-Sjögren syndrome (MSS), a debilitating autosomal recessive disease characterized by multisystem defects. A mouse model for MSS was previously produced by disrupting Sil1 using gene-trap methodology. The resulting Sil1Gt mouse phenocopies several pathologies associated with MSS, although its ability to assemble and secrete antibodies, the best-characterized substrate of BiP, has not been investigated. In vivo antigen-specific immunizations and ex vivo LPS stimulation of splenic B cells revealed that the Sil1Gt mouse was indistinguishable from wild-type age-matched controls in terms of both the kinetics and magnitude of antigen-specific antibody responses. There was no significant accumulation of BiP-associated Ig assembly intermediates or evidence that another molecular chaperone system was used for antibody production in the LPS-stimulated splenic B cells from Sil1Gt mice. ER chaperones were expressed at the same level in Sil1WT and Sil1Gt mice, indicating that there was no evident compensation for the disruption of Sil1. Finally, these results were confirmed and extended in three human EBV-transformed lymphoblastoid cell lines from individuals with MSS, leading us to conclude that the BiP cofactor Sil1 is dispensable for antibody production.
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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.