Z-DL-methionine
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Z-DL-methionine

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Category
CBZ-Amino Acids
Catalog number
BAT-003299
CAS number
4434-61-1
Molecular Formula
C13H17NO4S
Molecular Weight
283.40
Z-DL-methionine
IUPAC Name
4-methylsulfanyl-2-(phenylmethoxycarbonylamino)butanoic acid
Synonyms
Z-DL-Met-OH; N-Carbobenzoxy-DL-Methionine
Appearance
White to off-white powder
Purity
≥ 99% (HPLC)
Density
1.3 g/cm3
Melting Point
110-119 °C
Boiling Point
571.7°C
Storage
Store at 2-8°C
InChI
InChI=1S/C13H17NO4S/c1-19-8-7-11(12(15)16)14-13(17)18-9-10-5-3-2-4-6-10/h2-6,11H,7-9H2,1H3,(H,14,17)(H,15,16)
InChI Key
FPKHNNQXKZMOJJ-UHFFFAOYSA-N
Canonical SMILES
CSCCC(C(=O)O)NC(=O)OCC1=CC=CC=C1
1. Bioavailability of the dl-methionine and the calcium salt of dl-methionine hydroxy analog compared with l-methionine for nitrogen retention in starter pigs
Hua Zhou, Zhengcai Yuan, Daiwen Chen, Huifeng Wang, Yan Shu, Jun Gao, John Khun Htoo, Bing Yu J Anim Sci. 2021 Jun 1;99(6):skab151. doi: 10.1093/jas/skab151.
Two nitrogen balance studies were conducted to evaluate the relative bioavailability values (RBV) of dl-methionine (dl-Met) and dl-methionine hydroxy analog calcium salt (MHA-Ca) to l-methionine (l-Met) as Met sources fed to pigs. In experiment 1, 42 pigs were assigned to 7 treatments feeding with basal diet (BD) formulated to be deficient in Met (0.22% standardized ileal digestible basis) but adequate in other amino acids. Diets included (1) BD, (2) BD + 0.025% dl-Met, (3) BD + 0.050% dl-Met, (4) BD + 0.075% dl-Met, (5) BD + 0.025% l-Met, (6) BD + 0.050% l-Met, and (7) BD + 0.075% l-Met. Increasing levels of l-Met and dl-Met enhanced N retained (g/d) and N retention (% of intake) linearly (P < 0.01). Using a linear slope ratio procedure, a product-to-product RBV of dl-Met compared with l-Met was 94% (95% confidence limits: 65% to 123%) based on N retained expressed as g/d and 99% (95% confidence limits: 70% to 128%) for N retention expressed as % of intake. In experiment 2, 42 pigs were allotted to 7 treatments in another N-balance trial. Diets included (1) BD, (2) BD + 0.025% l-Met, (3) BD + 0.050% l-Met, (4) BD + 0.075% l-Met, (5) BD + 0.030% MHA-Ca, (6) BD + 0.060% MHA-Ca, and (7) BD + 0.089% MHA-Ca. An increase in dietary inclusion rates of l-Met increased (P < 0.01) N retained (g/d) linearly while increasing levels of MHA-Ca had no effects (P > 0.05) on N retained (g/d) and N retention (% of intake). Using linear slope-ratio regression, the RBV of MHA-Ca compared with l-Met was 70% (95% confidence limits: 59% to 81%) on a product-to-product basis or 83% on equimolar basis based on N retained expressed as g/d. Overall, the mean RBV of dl-Met to l-Met of 97% (95% confidence limits cover 100%) indicated that dl-Met and l-Met are equally bioavailable as Met sources in pigs. Compared with l-Met, the RBV of MHA-Ca was lower at 70% (95% confidence limits: 59% to 81%) on a product-to-product basis or 83% on equimolar basis in starter pigs.
2. The landscape of tumor cell states and spatial organization in H3-K27M mutant diffuse midline glioma across age and location
Ilon Liu, et al. Nat Genet. 2022 Dec;54(12):1881-1894. doi: 10.1038/s41588-022-01236-3. Epub 2022 Dec 5.
Histone 3 lysine27-to-methionine (H3-K27M) mutations most frequently occur in diffuse midline gliomas (DMGs) of the childhood pons but are also increasingly recognized in adults. Their potential heterogeneity at different ages and midline locations is vastly understudied. Here, through dissecting the single-cell transcriptomic, epigenomic and spatial architectures of a comprehensive cohort of patient H3-K27M DMGs, we delineate how age and anatomical location shape glioma cell-intrinsic and -extrinsic features in light of the shared driver mutation. We show that stem-like oligodendroglial precursor-like cells, present across all clinico-anatomical groups, display varying levels of maturation dependent on location. We reveal a previously underappreciated relationship between mesenchymal cancer cell states and age, linked to age-dependent differences in the immune microenvironment. Further, we resolve the spatial organization of H3-K27M DMG cell populations and identify a mitotic oligodendroglial-lineage niche. Collectively, our study provides a powerful framework for rational modeling and therapeutic interventions.
3. Somatic Mutations in UBA1 and Severe Adult-Onset Autoinflammatory Disease
David B Beck, et al. N Engl J Med. 2020 Dec 31;383(27):2628-2638. doi: 10.1056/NEJMoa2026834. Epub 2020 Oct 27.
Background: Adult-onset inflammatory syndromes often manifest with overlapping clinical features. Variants in ubiquitin-related genes, previously implicated in autoinflammatory disease, may define new disorders. Methods: We analyzed peripheral-blood exome sequence data independent of clinical phenotype and inheritance pattern to identify deleterious mutations in ubiquitin-related genes. Sanger sequencing, immunoblotting, immunohistochemical testing, flow cytometry, and transcriptome and cytokine profiling were performed. CRISPR-Cas9-edited zebrafish were used as an in vivo model to assess gene function. Results: We identified 25 men with somatic mutations affecting methionine-41 (p.Met41) in UBA1, the major E1 enzyme that initiates ubiquitylation. (The gene UBA1 lies on the X chromosome.) In such patients, an often fatal, treatment-refractory inflammatory syndrome develops in late adulthood, with fevers, cytopenias, characteristic vacuoles in myeloid and erythroid precursor cells, dysplastic bone marrow, neutrophilic cutaneous and pulmonary inflammation, chondritis, and vasculitis. Most of these 25 patients met clinical criteria for an inflammatory syndrome (relapsing polychondritis, Sweet's syndrome, polyarteritis nodosa, or giant-cell arteritis) or a hematologic condition (myelodysplastic syndrome or multiple myeloma) or both. Mutations were found in more than half the hematopoietic stem cells, including peripheral-blood myeloid cells but not lymphocytes or fibroblasts. Mutations affecting p.Met41 resulted in loss of the canonical cytoplasmic isoform of UBA1 and in expression of a novel, catalytically impaired isoform initiated at p.Met67. Mutant peripheral-blood cells showed decreased ubiquitylation and activated innate immune pathways. Knockout of the cytoplasmic UBA1 isoform homologue in zebrafish caused systemic inflammation. Conclusions: Using a genotype-driven approach, we identified a disorder that connects seemingly unrelated adult-onset inflammatory syndromes. We named this disorder the VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome. (Funded by the NIH Intramural Research Programs and the EU Horizon 2020 Research and Innovation Program.).
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