ArticleBiochimie2013
The C-terminal domain of CblD interacts with CblC and influences intracellular cobalamin partitioning.
Article in Biochimie, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Mitochondrial depolarization stabilizes the vitamin BProceedings of the National Academy of Sciences of the United States of America · 2026Article
- An unusual Co-S bond links BProceedings of the National Academy of Sciences of the United States of America · 2025Article
- From Nutrient to Nanocarrier: The Multifaceted Role of Vitamin B12 in Drug Delivery.International journal of molecular sciences · 2025Review
- The cobalamin processing enzyme of Trichoplax adhaerens.The Journal of biological chemistry · 2025Article
- Kinetics of Cellular Cobalamin Uptake and Conversion: Comparison of Aquo/Hydroxocobalamin to Cyanocobalamin.Nutrients · 2024Article
- Cobalt-Sulfur Coordination Chemistry Drives BJournal of the American Chemical Society · 2023Article
- Versatile enzymology and heterogeneous phenotypes in cobalamin complementation type C disease.iScience · 2022Review
- Redox-Linked Coordination Chemistry Directs Vitamin BAccounts of chemical research · 2021Article
- Utilization of cobalamin is ubiquitous in early-branching fungal phyla.Genome biology and evolution · 2021Article
- MMADHC premature termination codons in the pathogenesis of cobalamin D disorder: Potential of translational readthrough reconstitution.Molecular genetics and metabolism reports · 2021Article
- An Interprotein Co-S Coordination Complex in the BJournal of the American Chemical Society · 2020Article
- Catalytic effect of riboflavin on electron transfer from NADH to aquacobalamin.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2020Article
- Targeted Metabolic Profiling of Methionine Cycle Metabolites and Redox Thiol Pools in Mammalian Plasma, Cells and Urine.Metabolites · 2019Article
- Transcellular transport of cobalamin in aortic endothelial cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Cobalamin-Associated Superoxide Scavenging in Neuronal Cells Is a Potential Mechanism for Vitamin BThe American journal of pathology · 2018Article
- Structure of Human B12 Trafficking Protein CblD Reveals Molecular Mimicry and Identifies a New Subfamily of Nitro-FMN Reductases.The Journal of biological chemistry · 2015Article
- Structural Insights into the MMACHC-MMADHC Protein Complex Involved in Vitamin B12 Trafficking.The Journal of biological chemistry · 2015Article
- Characterization of functional domains of the cblD (MMADHC) gene product.Journal of inherited metabolic disease · 2014Article
- Glutathione-dependent one-electron transfer reactions catalyzed by a B₁₂ trafficking protein.The Journal of biological chemistry · 2014Article
- Clinical, Biochemical, and Molecular Presentation in a Patient with the cblD-Homocystinuria Inborn Error of Cobalamin Metabolism.JIMD reports · 2014Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Mutations in cobalamin or B12 trafficking genes needed for cofactor assimilation and targeting lead to inborn errors of cobalamin metabolism. The gene corresponding to one of these loci, cblD, affects both the mitochondrial and cytoplasmic pathways for B12 processing. We have demonstrated that fibroblast cell lines from patients with mutations in CblD, can dealkylate exogenously supplied methylcobalamin (MeCbl), an activity catalyzed by the CblC protein, but show imbalanced intracellular partitioning of the cofactor into the MeCbl and 5'-deoxyadenosylcobalamin (AdoCbl) pools. These results confirm that CblD functions downstream of CblC in the cofactor assimilation pathway and that it plays an important role in controlling the traffic of the cofactor between the competing cytoplasmic and mitochondrial routes for MeCbl and AdoCbl synthesis, respectively. In this study, we report the interaction of CblC with four CblD protein variants with variable N-terminal start sites. We demonstrate that a complex between CblC and CblD can be isolated particularly under conditions that permit dealkylation of alkylcobalamin by CblC or in the presence of the corresponding dealkylated and oxidized product, hydroxocobalamin (HOCbl). A weak CblC·CblD complex is also seen in the presence of cyanocobalamin. Formation of the CblC·CblD complex is observed with all four CblD variants tested suggesting that the N-terminal 115 residues missing in the shortest variant are not essential for this interaction. Furthermore, limited proteolysis of the CblD variants indicates the presence of a stable C-terminal domain spanning residues ∼116-296. Our results are consistent with an adapter function for CblD, which in complex with CblC·HOCbl, or possibly the less oxidized CblC·cob(II)alamin, partitions the cofactor between AdoCbl and MeCbl assimilation pathways.
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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.