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Update to Avantor’s response to the coronavirus (COVID-19) pandemic

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Pentafluorophenyl+isothiocyanate


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Supplier:  Bioss
Description:   Defects in G6PD are the cause of chronic non-spherocytic hemolytic anemia (CNSHA) . Deficiency of G6PD is associated with hemolytic anemia in two different situations. First, in areas in which malaria has been endemic, G6PD-deficiency alleles have reached high frequencies (1% to 50%) and deficient individuals, though essentially asymptomatic in the steady state, have a high risk of acute hemolytic attacks. Secondly, sporadic cases of G6PD deficiency occur at a very low frequencies, and they usually present a more severe phenotype. Several types of CNSHA are recognized. Class-I variants are associated with severe NSHA; class-II have an activity <10% of normal; class-III have an activity of 10% to 60% of normal; class-IV have near normal activity.
Supplier:  Bioss
Description:   Fibroblast growth factors (FGFs) produce mitogenic and angiogenic effects in target cells by signaling through the cellular surface tyrosine kinase receptors. There are four members of the FGF receptor family: FGFR-1 (flg), FGFR-2 (bek, KGFR), FGFR-3 and FGFR-4. Each receptor contains an extracellular ligand binding domain, a transmembrane region and a cytoplasmic kinase domain (1). Following ligand binding and dimerization, the receptors are phosphorylated at specific tyrosine residues (2). Seven tyrosine residues in the cytoplasmic tail of FGFR-1 can be phosphorylated: Tyr463, Tyr583, Tyr585, Tyr653, Tyr654, Tyr730 and Tyr766. Tyrosine 653 and 654 are important for catalytic activity of the activated FGFR and are essential for signaling (3). The other phosphorylated tyrosine residues may provide docking sites for downstream signaling components such as Crk and PLCgamma.
Supplier:  Bioss
Description:   Essential transmembrane GTPase, which mediates mitochondrial fusion. Fusion of mitochondria occurs in many cell types and constitutes an important step in mitochondria morphology, which is balanced between fusion and fission. MFN2 acts independently of the cytoskeleton. It therefore plays a central role in mitochondrial metabolism and may be associated with obesity and/or apoptosis processes. Overexpression induces the formation of mitochondrial networks. Plays an important role in the regulation of vascular smooth muscle cell proliferation. Involved in the clearance of damaged mitochondria via selective autophagy (mitophagy). Is required for PARK2 recruitment to dysfunctional mitochondria. Involved in the control of unfolded protein response (UPR) upon ER stress including activation of apoptosis and autophagy during ER stress. Acts as an upstream regulator of EIF2AK3 and suppresses EIF2AK3 activation under basal conditions.
Supplier:  Bioss
Description:   Poly-ADP-ribosyltransferase involved in various processes such as Wnt signaling pathway, telomere length and vesicle trafficking. Acts as an activator of the Wnt signaling pathway by mediating poly-ADP-ribosylation (PARsylation) of AXIN1 and AXIN2, 2 key components of the beta-catenin destruction complex: poly-ADP-ribosylated target proteins are recognized by RNF146, which mediates their ubiquitination and subsequent degradation. Also mediates PARsylation of BLZF1 and CASC3, followed by recruitment of RNF146 and subsequent ubiquitination. Mediates PARsylation of TERF1, thereby contributing to the regulation of telomere length. Involved in centrosome maturation during prometaphase by mediating PARsylation of HEPACAM2/MIKI. May also regulate vesicle trafficking and modulate the subcellular distribution of SLC2A4/GLUT4-vesicles. May be involved in spindle pole assembly through PARsylation of NUMA1. Stimulates 26S proteasome activity.
Supplier:  Bioss
Description:   GIMAP3p is a murine mitochondrial membrane protein belonging to the GTP-binding superfamily and to the immuno-associated nucleotide (IAN) subfamily of nucleotide-binding proteins. The IAN/GIMAP family consists of GTP-binding proteins that share a unique primary structure and whose expression is finely regulated by T-cell receptor signals. Recent studies have shown that IAN/GIMAP family proteins crucially regulate the survival of T cells during development, selection and homeostasis, and are possibly linked to the onset of T-lymphopenia, leukemia and autoimmunity. IAN/GIMAP family proteins might also take part in mitochondrial regulation of lymphocyte apoptosis by interacting with Bcl-2 family proteins. The human GIMAP (GTPase of the immunity-associated protein) gene family includes seven functional members residing on (human) chromosome 7q36.1 and one pseudogene (hGIMAP3).
Supplier:  Bioss
Description:   RORET, also known as RING finger protein 15 (RNF15) or zinc finger protein RoRet, is a 465 amino acid member of the TRIM family, also known as the RING-B-box coiled-coil (RBCC) family. Members of the RBCC family have an N-terminal RING finger, followed by one or two zinc-binding domains (B-box domains), a leucine coiled-coil region and a variable C-terminal domain. Found in all eukaryotes, members of the RBCC family typically function within a larger protein complex and possess ubiquitin-protein isopeptide ligase activity.The protein encoded by this gene is a member of the tripartite motif (TRIM) family. The TRIM motif includes three zinc-binding domains, a RING, a B-box type 1 and a B-box type 2, and a coiled-coil region. The function of this protein has not been identified.
Supplier:  Bioss
Description:   Schlafen family members are preferentially expressed in lymphoid tissues and are differentially regulated during thymocyte maturation. Schlafen proteins function as suppressors of cell growth and are thought to play a role in the maintenance of T cell quiescence. The prototype member of the Schlafen family, Slfn1, is transcriptionally unregulated during thymocyte positive selection, and the induction of Slfn1 induces a G0/G1 arrest, suggesting that Slfn1 participates in the regulation of cell cycle and potentially acts as a determining factor for apoptosis. These proteins all contain a largely conserved core domain within the center of the sequence, and yet they are substantially diversified at the N terminus. Slfn14 (Schlafen family member 14) is a 912 amino acid protein belonging to the Schlafen family. Slfn14 exists as two alternatively spliced isoforms and is encoded by a gene mapping to human chromosome 17q12.
Supplier:  Bioss
Description:   Encoding more than 700 genes, chromosome 15 is made up of approximately 106 million base pairs and is about 3% of the human genome. Angelman and Prader-Willi syndromes are associated with loss of function or deletion of genes in the 15q11-q13 region. In the case of Angelman syndrome, this loss is due to inactivity of the maternal 15q11-q13 encoded UBE3A gene in the brain by either chromosomal deletion or mutation. In cases of Prader-Willi syndrome, there is a partial or complete deletion of this region from the paternal copy of chromosome 15. Tay-Sachs disease is a lethal disorder associated with mutations of the HEXA gene, which is encoded by chromosome 15. Marfan syndrome is associated with chromosome 15 through the FBN1 gene. The FAM81A gene product has been provisionally designated FAM81A pending further characterization.
Supplier:  Bioss
Description:   Ubiquitination is an important mechanism through which three classes of enzymes act in concert to target short-lived or abnormal proteins for destruction. The three classes of enzymes involved in ubiquitination are the ubiquitin-activating enzymes (E1s), the ubiquitin-conjugating enzymes (E2s) and the ubiquitin-protein ligases (E3s). UBC13, also known as UBE2N or BLU, is a 152 amino acid member of the E2 ubiquitin-conjugating enzyme family. Existing as a heterodimer with Mms2 (also known as UBE2V2), UBC13 catalyzes the ATP-dependent synthesis of non-canonical polyubiquitin chains, a process that does not lead to proteasomal degradation. Additionally, UBC13 mediates the transcription of several target genes and is thought to play a role in cell cycle progression, cellular differentiation and DNA repair mechanisms that ensure cell survival after DNA damage.
Supplier:  Bioss
Description:   SLAMF7 contains one Ig-like C2-type (immunoglobulin-like) domain. Isoform 1 mediates NK cell activation through a SAP-independent extracellular signal-regulated ERK-mediated pathway. It may play a role in lymphocyte adhesion. Isoform 3 does not mediate any activation. SAP can bind the cytoplasmic tail of isoform 1 when phosphorylated in the presence of Fyn (in vitro). SLAMF7 is expressed in spleen, lymph node, peripheral blood leukocytes, bone marrow, small intestine, stomach, appendix, lung and trachea. Expression was detected in NK cells, activated B-cells, NK-cell line but not in promyelocytic, B-, or T-cell lines. The isoform 3 is expressed at much lower level than isoform 1. There are three named isoforms.
Supplier:  Bioss
Description:   Apoptosis, or programmed cell death, occurs during normal cellular differentiation and development of multicellular organisms. Apoptosis is induced by certain cytokines including TNF and Fas ligand of the TNF family through their death domain containing receptors, TNFR1 and Fas. Cell death signals are transduced by death domain (DD) containing adapter molecules and members of the ICE/CED3 protease family. A novel DD containing molecule was recently cloned from mouse, human and monkey and designated Daxx. Daxx is a death domain containing important intermediate in the Fas mediated apoptosis. Daxx binds specifically to the Fas death domain and enhances Fas induced apoptosis and activates the Jun N terminal kinase (JNK) pathway. It is widely expressed in fetal and adult human and mouse tissue, indicating its important function in Fas signaling pathways.
Supplier:  Bioss
Description:   ADAMTS proteases are secreted enzymes containing a prometalloprotease domain of the reprolysin type. The ADAMTS proteases function in processing of procollagens and von Willebrand factor as well as catabolism of aggrecan, versican and brevican. They have been demonstrated to have important roles in connective tissue organization, coagulation, inflammation, arthritis, angiogenesis and cell migration.A member of the metalloproteinase family containing disintegrin like domains (ADAMs), the function of ADAMTS8 is still poorly understood. ADAMTS8 contains the canonical HExxHxxxxxH zinc metalloproteinase motif, and has been shown to be proteolytically active on a range of substrates. ADAMTS8 is inhibited by the endogenous MMP inhibitors, TIMP1, 2, 3 and 4, but most efficiently by TIMP3. In addition to the metalloprotease domain, ADAMTS8 has a propeptide domain, a Prohormone Convertase (PC, furin) cleavage site, a cysteine rich domain and thrombospondin 1 like domains.
Supplier:  Bioss
Description:   Made up of nearly 146 million bases, chromosome 8 encodes about 800 genes. Translocation of portions of chromosome 8 with amplifications of the c-Myc gene are found in some leukemias and lymphomas, and typically associated with a poor prognosis. Portions of chromosome 8 have been linked to schizophrenia and bipolar disorder. Trisomy 8, also known as Warkany syndrome 2, most often results in early miscarriage but is occasionally seen in a mosaic form in surviving patients who suffer to a varying degree from a number of symptoms including retarded mental and motor development, and certain facial and developmental defects. WRN is a DNA helicase encoded by chromosome 8 and shown defective in those with the early aging disorder Werner syndrome. Chromosome 8 is also associated with Pfeiffer syndrome, congenital hypothyroidism and Waardenburg syndrome.
Supplier:  Bioss
Description:   Involved in adaptive response to hypoxia. Suppresses hypoxia-inducible expression of HIF1A and EPAS1. Binds to core DNA sequence 5'-TACGTG-3' within the hypoxia response element (HRE) of target gene promoters. The complex HIF3A-ARNT activates the transcription of reporter genes driven by HRE. Isoform 4 has a dominant-negative function of inactivating HIF1A-mediated transcription. Isoform 4 attenuates the binding of HIF1A to hypoxia-responsive elements (HRE), thus inhibiting HRE-driven transcription. Hypoxia induces down-regulation of isoform 4, leading to activation of HIF1A in hypoxia. Conversely, upon restoring normoxia, the expression of isoform 4 increases and thereby secure an inhibition of HIF1A activity. Isoform 4 may be a negative regulator of hypoxia-inducible gene expression in the kidney and may be involved in renal tumorigenesis. Functions as an inhibitor of angiogenesis in the cornea (By similarity).
Supplier:  Bioss
Description:   FBXO15, also known as FBX15, is a 434 amino acid protein that contains one C-terminal F-box domain and belongs to the F-box family of proteins. F-box proteins are critical components of the SCF (Skp1-CUL-1-F-box protein) type E3 ubiquitin ligase complex and are involved in substrate recognition and recruitment for ubiquitination. They are members of a larger family of proteins that are involved in the regulation of a wide variety of cellular processes (including the cell cycle, immune response, signaling cascades and developmental processes) through the targeting of proteins, such as cyclins, cyclin-dependent kinase inhibitors, IkB-a and b-catenin, for degradation by the proteasome after ubiquitination. Via its F-box domain, FBXO15 can directly interact with Skp1 p19 and CUL-1. In addition, FBXO15 is a target of the transcription factor Oct-3/4, however, it does not appear to be essential for early development and fertility.
Supplier:  Bioss
Description:   The finding that mutations in DNA mismatch repair genes are associated with hereditary nonpolyposis colorectal cancer (HNPCC) has resulted in considerable interest in the understanding of the mechanism of DNA mismatch repair. Initially, inherited mutations in the MSH2 and MLH1 homologs of the bacterial DNA mismatch repair genes MutS and MutL were demonstrated at high frequency in HNPCC and were shown to be associated with microsatellite instability. The demonstration that 10 to 45% of pancreatic, gastric, breast, ovarian and small cell lung cancers also display microsatellite instability has been interpreted to suggest that DNA mismatch repair is not restricted to HNPCC tumors but is a common feature in tumor initiation or progression. Two additional homologs of the prokaryotic MutL gene, designated PMS1 and PMS2, have been identified and shown to be mutated in the germline of HNPCC patients.
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