Fmoc-L-Lys(Ac)-AMC
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Fmoc-L-Lys(Ac)-AMC

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Category
Fmoc-Amino Acids
Catalog number
BAT-008476
CAS number
787549-21-7
Molecular Formula
C33H33N3O6
Molecular Weight
567.63
IUPAC Name
(S)-(9H-fluoren-9-yl)methyl (6-acetamido-1-((4-methyl-2-oxo-2H-chromen-7-yl)amino)-1-oxohexan-2-yl)carbamate
InChI
InChI=1S/C33H33N3O6/c1-20-17-31(38)42-30-18-22(14-15-23(20)30)35-32(39)29(13-7-8-16-34-21(2)37)36-33(40)41-19-28-26-11-5-3-9-24(26)25-10-4-6-12-27(25)28/h3-6,9-12,14-15,17-18,28-29H,7-8,13,16,19H2,1-2H3,(H,34,37)(H,35,39)(H,36,40)/t29-/m0/s1
InChI Key
HZTZGAGMLJWGEJ-LJAQVGFWSA-N
Canonical SMILES
CC1=CC(=O)OC2=C1C=CC(=C2)NC(=O)C(CCCCNC(=O)C)NC(=O)OCC3C4=CC=CC=C4C5=CC=CC=C35
1. PI3Kδ and primary immunodeficiencies
Carrie L Lucas, Anita Chandra, Sergey Nejentsev, Alison M Condliffe, Klaus Okkenhaug Nat Rev Immunol. 2016 Nov;16(11):702-714. doi: 10.1038/nri.2016.93. Epub 2016 Sep 12.
Primary immunodeficiencies are inherited disorders of the immune system, often caused by the mutation of genes required for lymphocyte development and activation. Recently, several studies have identified gain-of-function mutations in the phosphoinositide 3-kinase (PI3K) genes PIK3CD (which encodes p110δ) and PIK3R1 (which encodes p85α) that cause a combined immunodeficiency syndrome, referred to as activated PI3Kδ syndrome (APDS; also known as p110δ-activating mutation causing senescent T cells, lymphadenopathy and immunodeficiency (PASLI)). Paradoxically, both loss-of-function and gain-of-function mutations that affect these genes lead to immunosuppression, albeit via different mechanisms. Here, we review the roles of PI3Kδ in adaptive immunity, describe the clinical manifestations and mechanisms of disease in APDS and highlight new insights into PI3Kδ gleaned from these patients, as well as implications of these findings for clinical therapy.
2. Immunophenotyping of COVID-19 and influenza highlights the role of type I interferons in development of severe COVID-19
Jeong Seok Lee, et al. Sci Immunol. 2020 Jul 10;5(49):eabd1554. doi: 10.1126/sciimmunol.abd1554.
Although most SARS-CoV-2-infected individuals experience mild coronavirus disease 2019 (COVID-19), some patients suffer from severe COVID-19, which is accompanied by acute respiratory distress syndrome and systemic inflammation. To identify factors driving severe progression of COVID-19, we performed single-cell RNA-seq using peripheral blood mononuclear cells (PBMCs) obtained from healthy donors, patients with mild or severe COVID-19, and patients with severe influenza. Patients with COVID-19 exhibited hyper-inflammatory signatures across all types of cells among PBMCs, particularly up-regulation of the TNF/IL-1β-driven inflammatory response as compared to severe influenza. In classical monocytes from patients with severe COVID-19, type I IFN response co-existed with the TNF/IL-1β-driven inflammation, and this was not seen in patients with milder COVID-19. Interestingly, we documented type I IFN-driven inflammatory features in patients with severe influenza as well. Based on this, we propose that the type I IFN response plays a pivotal role in exacerbating inflammation in severe COVID-19.
3. Genomic landscape of colorectal carcinogenesis
Jin Cheon Kim, Walter F Bodmer J Cancer Res Clin Oncol. 2022 Mar;148(3):533-545. doi: 10.1007/s00432-021-03888-w. Epub 2022 Jan 20.
Purpose: The molecular pathogenesis of solid tumour was first assessed in colorectal cancer (CRC). To date, ≤ 100 genes with somatic alterations have been found to inter-connectively promote neoplastic transformation through specific pathways. The process of colorectal carcinogenesis via genome landscape is reviewed on the basis of an adenoma-to-carcinoma sequence, as shown by serial histological and epidemiological observations. Methods: The relevant literatures from PubMed (1980-2021) have been reviewed for this article. Results: The major routes of CRC development, chromosomal instability (CIN), microsatellite instability (MSI), and the serrated route either via CIN or MSI, proceed through the respective molecular pathway of colorectal carcinogenesis. Particular aspects of CRC carcinogenesis can also be determined by evaluating familial CRCs (FCRC) and genotype-phenotype correlations. Specific causative gene alterations still leave to be identified in several FCRCs. Otherwise, recently verified FCRC can be particularly notable, for example, EPCAM-associated Lynch syndrome, polymerase proofreading-associated polyposis, RNF43-associated polyposis syndrome or NTHL1 tumour syndrome, and hereditary mixed polyposis syndrome. The oncogenic landscape is described, including representative pathway genes, the three routes of carcinogenesis, familial CRCs, genotype-phenotype correlations, the identification of causative genes, and consensus molecular subtypes (CMS). Conclusion: Whole genome research using multi-gene panels (MGPs) has facilitated high through-put detection of previously unidentified genes involved in colorectal carcinogenesis. New approaches designed to identify rare variants are recommended to consider their alterations implicated in the molecular pathogenesis.
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