Abstract. HIV-1 tat targets a variety of host cell proteins to facilitate viral transcription and disrupts host cellular immunity by inducing lymphocyte apoptosis, but whether it influences humoral immunity remains unclear. Previously, our group demonstrated that tat depresses expression of DNA-PKcs, a critical component of the non-homologous end joining pathway (NHEJ) of DNA double-strand breaks repair, immunoglobulin class switch recombination (CSR) and V(D)J recombination, and sensitizes cells to ionizing radiation. In this study, we demonstrated that HIV-1 Tat down-regulates DNA-PKcs expression by directly binding to the core promoter sequence. In addition, Tat interacts with and activates the kinase activity of DNA-PKcs in a dose-dependent and DNA independent manner. Furthermore, Tat inhibits class switch recombination (CSR) at low concentrations (≤4 µg/ml) and stimulates CSR at high concentrations (≥8 µg/ml). On the other hand, low protein level and high kinase activity of DNA-PKcs ...
DNA double-strand breaks (DSBs) represent serious threats to cell survival, and inappropriate response to this threat may lead to genome instability and development of cancer. DSBs can be caused by exogenous agents such as ionizing radiation or certain chemicals, but can also arise during normal endogenous processes, including DNA replication and meiosis. There are two major pathways for repair of DSBs: homologous recombination (HR) and nonhomologous end-joining (NHEJ). The former is dependent on sequence homology, is error free, and is most active in the late S/G2 phase of the cell cycle. The latter utilizes little, or no, sequence homology, is often imprecise, functions throughout the cell cycle, and is considered to be the principle mechanism used in vertebrate cells (1, 2). The classical NHEJ machinery requires a set of proteins, including Ku70, Ku80, DNA-PKcs, DNA ligase IV, XRCC4, Artemis and the recently identified XLF (Cernunnos) (3, 4). Alternative, or backup, NHEJ pathway(s), usually ...
Immunoglobulin heavy chain (IgH) class switch recombination (CSR) replaces the initially expressed IgH C exons with a set of downstream IgH constant region (CH) exons. functioned similarly to a size-matched synthetic S1 series to mediate significant CSR to IgG1 in mutant B cells turned on under circumstances that stimulate IgG1 switching in WT B cells. We conclude that S3 can function to S1 in mediating endogenous CSR to IgG1 similarly. The approach that people are suffering from will facilitate assays for IgH isotypeCspecific features of various other endogenous S locations. The IgH continuous area (CH) determines the course and effector features of immunoglobulins. IgH course change recombination (CSR) enables turned on B cells to change from creation of IgM to various other Ig classes, including IgG, IgE, and IgA. In mice, the exons that encode different IgH classes (termed CH LDN193189 genes) are arranged as 5CVDJCCCCCC3CC1CC2bCC2CCCCC3 (1). Each CH gene that goes through CSR is normally ...
We have developed a method for enumerating the frequency of Ig isotype switching in clones of B cells. The method adapts Poisson statistics to analyze the distribution of amounts of switched isotype produced by multiple subclones of cells and thus enables one to estimate the probability that a single cell will switch isotype in one cell generation. We have applied this method to determine the spontaneous switch frequency of two Ly-1+ B cell lymphomas of B10-H-2aH-4bp/Wts mice. Both CH12.LX and CH27.LX switch from IgM to IgA at very high frequencies (1 - 5 x 10-3 switch events per cell division) and from IgM to IgG at low but detectable frequencies (10-4 - 10-5 switch events per cell division). Cloned IgG variants of CH12.LX switch to IgA at the same frequency as the IgM-producing cells. Bacterial lipopolysaccharide has a strong inhibitory effect on isotype switching by CH12.LX. Possible explanations for the observed preference for switching to IgA are discussed ...
The time when the Th1 and Th2 cytokine profiles, respectively, start to develop in response to MMTV(SW) and NP-CGG has been determined by assessing the time when IL-4 and IFN-γ message increases in primary immune responses. This occurs during the third day after immunization when T cells first start to proliferate in association with interdigitating dendritic cells ((26)). Cognate interaction between T and B cells leading to B cell growth and the production of switch transcripts occurs on the same day, presumably shortly after the onset of T cell priming. The functional significance of the switch transcripts observed is indicated by the development of switched plasmablasts by day 5 after immunization. In the response to NP-CGG it is theoretically possible that T cell priming started before the onset of a detectable increase in T cell proliferation. This could apply if the number of antigen-reactive T cells initially was very low. This reservation does not apply to the response to MMTV(SW) where ...
Enables automatic analysis of class switch recombination (CSR) junctions sequenced by high-throughput sequencing (HTS). CSReport is a method able to support analysis of large numbers of sequences, with the aim of facilitating the manipulation and the extraction of valuable information. This program is composed of an algorithm that permits interpretation of each read as an assembly of a segment from the donor.
The concept behind HORIBAs CSR initiative is to fulfill our CSR through our business operations. Moreover, our stakeholders now expect more from us. We contribute to society in order to fulfill the role expected of us as a corporate citizen. It is important that HORIBAs significant awareness of, and initiatives to support CSR become well known by our stakeholders through our actions.. The HORIBA Group formed the HORIBA CSR Promotion Committee in April 2005; it is currently engaged in CSR initiatives with the full-fledged support of the Group companies ...
Generating your FileZilla CSR with OpenSSL. Easy instructions to create your CSR (certificate signing request) for FileZilla server using OpenSSL.
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Activation-induced cytidine deaminase (AID) is critical in normal B cells to initiate somatic hypermutation and immunoglobulin class switch recombination. Accumulating evidence suggests that AID is also prooncogenic, inducing cancer-promoting mutations or chromosome rearrangements. In this context, we find that AID is expressed in |40% of primary human chronic lymphocytic leukemia (CLL) cases, consistent with other reports. Using a combination of human B lymphoid leukemia cells and mouse models, we now show that AID expression can be harnessed for antileukemic effect, after inhibition of the RAD51 homologous recombination (HR) factor with 4,4-diisothiocyanatostilbene-2-2-disulfonic acid (DIDS). As a proof of principle, we show that DIDS treatment inhibits repair of AID-initiated DNA breaks, induces apoptosis, and promotes cytotoxicity preferentially in AID-expressing human CLL. This reveals a novel antineoplastic role of AID that can be triggered by inhibition of HR, suggesting a potential new
Antibody diversification through somatic hypermutation (SHM) and class switch recombination (CSR) are similarly initiated in B cells with the generation of U:G mismatches by activation-induced cytidine deaminase but differ in their subsequent mutagenic consequences. Although SHM relies on the generation of nondeleterious point mutations, CSR depends on the production of DNA double-strand breaks (DSBs) and their adequate recombination through nonhomologous end joining (NHEJ). MLH1, an ATPase member of the mismatch repair (MMR) machinery, is emerging as a likely regulator of whether a U:G mismatch progresses toward mutation or DSB formation. We conducted experiments on cancer modeled ATPase-deficient MLH1G67R knockin mice to determine the function that the ATPase domain of MLH1 mediates in SHM and CSR. Mlh1(GR/GR) mice displayed a significant decrease in CSR, mainly attributed to a reduction in the generation of DSBs and diminished accumulation of 53BP1 at the immunoglobulin switch regions. ...
To the best of our knowledge, this study is the first report suggesting a molecular mechanism by which heme regulates humoral immunity. Together with our recent report,15 our present results provide strong evidence that heme augments plasma cell differentiation by inhibiting Bach2, and thus increasing the population of Blimp-1-expressing cells. Because Blimp-1 is the master regulator of plasma cell differentiation,19,41 its derepression by heme through Bach2 inactivation may fine-tune the response of humoral immunity. In addition, heme may regulate the B-cell responses by inducing the expression of HO-1, which possesses antioxidant and immunomodulatory functions.9. In the spectral analyses, the 432-nm absorption band (6-coordinate heme-binding mode) and the 366-nm absorption band (5-coordinate heme-binding mode) both became apparent on addition of heme (Figure 1B). These results suggested that Bach2 bound to heme directly and had at least 2 distinct binding modes. Moreover, the spectral changes ...
Induced overexpression of AID in CH12F3-2 B lymphoma cells augmented class switching from IgM to IgA without cytokine stimulation. AID deficiency caused a complete defect in class switching and showed a hyper-IgM phenotype with enlarged germinal centers containing strongly activated B cells before o …
By creating an extremely diverse antibody repertoire, B cells protect the body against numerous infectious pathogens. Generation of this antibody repertoire depends on immunoglobulin gene modification events driven by four different molecular processes: V(D)J recombination, somatic hypermutation, class switch recombination, and gene conversion. The enzyme AID (activation-induced cytidine deaminase) is known to be involved in somatic hypermutation and class switch recombination. In their Perspective, Fugmann and Schatz explain that AID is also essential for gene conversion ( Arakawa et al.) and discuss how AID could operate in these three quite different processes. ...
Research group The research group of Prof. Qiang Pan-Hammarström works on the molecular mechanism of immunoglobulin class switch recombination (CSR), genetics of primary immunodeficiency and B-cell lymphomagenesis. The research laboratory is located at campus Flemingsberg. For more information about the group, please see https://ki.se/en/bionut/research-group-qiang-pan-hammarstrom Duties The selected postdoctoral fellow candidate will work in our multidisciplinary team of researchers including clinicians, molecular biologists and bioinformaticians, and will be jointly supervised by Prof. Qiang Pan-Hammarström at Karolinska Institutet (KI) and Prof. Feng Zhang at the Broad Institute at MIT and Harvard. The postdoctoral study will be primary based in KI, but will have possibilities to visit Broad Institute in Cambridge for additional training in technology and bioinformatics. The main tasks for the successful candidate are: 1) Characterization of RNA editing events in cells from healthy individuals as
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CSR is dependent on the rate of switch region transcription, and recombination is targeted to individual switch regions by transcription from intronic (I) promoters located upstream of each switch region. To determine if sterile transcription is normal in 53BP1−/− B cells, we measured the relative amounts of the μ and γ1 preswitch sterile transcripts (Reina-San-Martin et al., 2003) by quantitative real-time RT-PCR. As shown in Fig. 5 C, μ and γ1 sterile transcripts were expressed at comparable levels in wild-type and 53BP1−/− B cells, suggesting that sterile transcription of the IgM and IgG1 switch regions is not altered in the absence of 53BP1.. CSR is a deletional recombination reaction that results in the looping out and deletion of intervening DNA sequences as a circular episome (Iwasato et al., 1990; Matsuoka et al., 1990; von Schwedler et al., 1990). The looped-out circular DNA contains segments of Sμ and the target S region, including its I promoter. This promoter is still ...
Our system to produce antibodies is critical for our survival against numerous infections, but it causes also many tumors. B-lymphocytes can modify their immunoglobulin (Ig) genes to generate specific antibodies with a new isotype and enhanced affinity against an antigen. Activation-induced cytidine deaminase (AID) is the key mutagenic enzyme that initiates these processes by deaminating cytosine to uracil. How somatic hypermutation (SH) and class switch recombination (CSR) are targeted is key to understanding the defect DNA integrity in lymphomas and also in other tumors where inflammatory signals aberrantly induces AID. The trans-acting factors mediating specific targeting of AID and thereby SH and CSR have remained elusive. Here we show that mutant E2A with defect inhibition by the Ca2+sensor protein calmodulin results in reduced B cell receptor- (BCR-), IL4-plus CD40 ligand-stimulated CSR to IgE and instead aberrant CSR. AID is shown to be together with the transcription factors E2A, ...
The CLL genome is largely devoid of the chromosomal translocations and aberrant somatic hypermutations that are involved in several B cell non-Hodgkin lymphomas (B-NHLs) (1, 2, 49, 50, 53). These observation are consistent with a post-GC or GC-independent derivation of CLL because B-NHL-associated translocations are caused by errors during somatic hypermutation and class switch recombination, two mechanisms that are active in GC B cells (23). NGS studies have further elucidated the genomic complexity of CLLs and have shown that the average number of non-silent mutations (i.e., mutations that alter the protein sequence) per case is 10-12 at diagnosis, whereas the average number of copy number abnormalities is approximately two (45, 46, 51, 52). The order of magnitude of lesions detected in the coding genome of CLL appears considerably lower than in common epithelial cancers (54). Among hematologic malignancies, the complexity of the CLL genome is also on the lower side, markedly smaller than ...
Video articles in JoVE about immunoglobulin isotypes include Antibody Binding Specificity for Kappa (Vκ) Light Chain-containing Human (IgM) Antibodies: Polysialic Acid (PSA) Attached to NCAM as a Case Study, Techniques for the Analysis of Extracellular Vesicles Using Flow Cytometry, Antibody Labeling with Fluorescent Dyes Using Magnetic Protein A and Protein G Beads, Detection of True IgE-expressing Mouse B Lineage Cells, The Isolation, Differentiation, and Quantification of Human Antibody-secreting B Cells from Blood: ELISpot as a Functional Readout of Humoral Immunity, Induction and Assessment of Class Switch Recombination in Purified Murine B Cells, Generation of Murine Monoclonal Antibodies by Hybridoma Technology, Isolation and Characterization Of Chimeric Human Fc-expressing Proteins Using Protein A Membrane Adsorbers And A Streamlined Workflow, Colorectal Cancer Cell Surface Protein Profiling Using an Antibody Microarray and Fluorescence Multiplexing, Isolation of Primary
Sμ-Sα junction sequences. (A) Percentage of switch junctions with the indicated length of microhomology (excluding nucleotide additions). (B and C) Alignmen
Evaluation of the Ig isotype specificity of the FcμR. (A) FcμR cDNA-transduced BW5147 T cells were preincubated with various concentrations of inhibitor par
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There is a pretty common problem with the Fanatec CSR standard pedals. The pedal set send little spikes of input to the game and it auto calibrates...
TY - JOUR. T1 - Ubiquitylated PCNA plays a role in somatic hypermutation and class-switch recombination and is required for meiotic progression. AU - Roa, Sergio. AU - Avdievich, Elena. AU - Peled, Jonathan U.. AU - MacCarthy, Thomas. AU - Werling, Uwe. AU - Fei, Li Kuang. AU - Kan, Rui. AU - Zhao, Chunfang. AU - Bergman, Aviv. AU - Cohen, Paula E.. AU - Edelmann, Winfried. AU - Scharff, Matthew D.. PY - 2008/10/21. Y1 - 2008/10/21. N2 - Somatic hypermutation (SHM) and class-switch recombination (CSR) of Ig genes are dependent upon activation-induced cytidine deaminase (AID)-induced mutations. The scaffolding properties of proliferating cell nuclear antigen (PCNA) and ubiquitylation of its residue K164 have been suggested to play an important role organizing the error-prone repair events that contribute to the AID-induced diversification of the Ig locus. We generated knockout mice for PCNA (Pcna-/-), which were embryonic lethal. Expression of PCNA with the K164R mutation rescued the lethal ...
Affinity maturation and class switching of antibodies requires activation-induced cytidine deaminase (AID)-dependent hypermutation of Ig V(D)J rearrangements and Ig S areas, respectively, in activated B cells. in DT40 cells elevated the pace of AID-induced BMS-754807 gene conversion as much as 5-collapse. Furthermore, DNA-PKcs-deficiency appeared to reduce point mutation. The data provide strong evidence that double-strand DNA ends capable of recruiting the DNA-dependent protein kinase complex are important intermediates in Ig V gene conversion. Author Summary To generate highly specific antibodies in response to an immune challenge, the antibody genes in triggered B cells mutate at a very high rate over a period of several days. The enzyme that initiates antibody gene mutation is definitely activation-induced cytidine deaminase (AID), the 1st protein recognized to directly edit DNA genomes BMS-754807 in vivo. AID induces point mutation of antibody V genes in all vertebrates, as well as transfer ...
Activation-induced cytidine deaminase (AID) was discovered by Muramatsu et al. (7) as an APOBEC1 homolog with cytidine deaminase properties in stimulated B cell lines. Muramatsu et al. (8) showed that AID is necessary for somatic hypermutation and class switch recombination, because AID−/− B lymphocytes do not undergo class switch recombination and fail to accumulate mutations upon Ag stimulation. Mutations in the human AID gene causing lack of function underlie one type of hyper-IgM syndrome. In this syndrome, B cells fail to switch from IgM to other isotypes, and somatic hypermutation of the Ig V regions does not occur (9). This syndrome seemingly connects AID with Ig isotype class switch and somatic hypermutation. Arakawa et al. (10) demonstrated that AID is also required for Ig gene conversion in chicken B cell lines. Thus, AID participates in three different processes that contribute to the diversification of Abs: somatic hypermutation, isotype class switch recombination, and gene ...
Activation-induced deaminase (AID) is expressed only in germinal center B cells. There, it is required for somatic hypermutation, gene conversion and class switch recombination of antibody variable region segments, three processes that diversify antibodies during immune responses. Although AID has homology to RNA-editing enzymes, three recent reports suggest it could initiate the diversification processes by deaminating cytidine residues within the antibody genes themselves.
Putative catalytic component of the RNA exosome complex which has 3->5 exoribonuclease activity and participates in a multitude of cellular RNA processing and degradation events. In the nucleus, the RNA exosome complex is involved in proper maturation of stable RNA species such as rRNA, snRNA and snoRNA, in the elimination of RNA processing by-products and non-coding pervasive transcripts, such as antisense RNA species and promoter-upstream transcripts (PROMPTs), and of mRNAs with processing defects, thereby limiting or excluding their export to the cytoplasm. The RNA exosome may be involved in Ig class switch recombination (CSR) and/or Ig variable region somatic hypermutation (SHM) by targeting AICDA deamination activity to transcribed dsDNA substrates. In the cytoplasm, the RNA exosome complex is involved in general mRNA turnover and specifically degrades inherently unstable mRNAs containing AU-rich elements (AREs) within their 3 untranslated regions, and in RNA surveillance pathways, preventing
Activation-induced deaminase (AID) initiates somatic hypermutation (SHM) and class switch recombination (CSR) by inducing mutations and double-strand breaks at the immunoglobulin (Ig) locus in B cells. AID converts deoxycytidine (dC) to deoxyuridine (dU) in single-stranded DNA (ssDNA). This deaminat …
Our laboratory is studying how antibody-forming cells respond to antigen by undergoing somatic hypermutation and class switch recombination so that they can produce higher affinity antibodies with more useful effector functions. The molecular and biochemical mechanisms of antibody variable region hypermutation and class switch recombination is being studied in mice that have mutations in various repair proteins in collaboration with Dr. Winfried Edelmann. In order to examine detailed molecular mechanisms, we are also studying how mutation is targeted to antibody genes and some oncogenes in human Burkitts lymphoma cell lines which are undergoing variable region mutation in culture. These cell lines and genetically defective mice are being used to study the role of activation induced deaminase (AID), mismatch repair and error prone polymerases in the variable region hypermutation and isotype switching. The analysis of these events also involves the examination of AID activity biochemically and, ...
Activation-induced cytidine deaminase (AID) is the key mutagenic enzyme that initiates somatic hypermutation (SH) and class switch recombination (CSR) by deaminating cytosine to uracil. The targeting of AID and therefore SH and CSR to Ig genes is a central process of the immune system, but the trans-acting factors mediating the specific targeting have remained elusive. Here we show that defective calmodulin inhibition of the transcription factor E2A after activation of the B cell receptor (BCR) leads to reduced BCR, IL4 plus CD40 ligand stimulated CSR to IgE and instead CSR to other Ig classes. AID that initiates CSR is shown to be in a complex with the transcription factors E2A, PAX5 and IRF4 on key sequences of the Igh locus. Calmodulin shows proximity with each of them after BCR stimulation. BCR signaling reduces binding of the proteins to some of the target sites on the Igh locus, and calmodulin resistance of E2A blocks these reductions. AID binds directly to the bHLH domain of E2A and to ...
Activation-induced cytidine deaminase (AID) is essential for two processes of immunoglobulin diversification in germinal center B cells: somatic hypermutation (SHM), in which mutations are introduced into immunoglobulin (Ig) genes, and class-switch recombination (CSR), in which genomic constant regions are recombined to encode antibodies of different isotypes. Both of these processes require AID-catalyzed C-to-U lesions at the Ig loci, which are resolved to generate point mutations or double-stranded DNA breaks in the cases of SHM and CSR, respectively. Despite over a decade of intense study, a number of open issues remain surrounding AID. The diversity of findings regarding AIDs role in DNA demethylation raises the question of the scope of its involvement in this process. Additionally, while it is clear that AID-mediated damage occurs, the effects of this damage on the average B cell have not been characterized. Finally, the issue of whether AID is able to edit RNA in vivo has never been rigorously
During B cell activation, the DNA lesions that initiate somatic hypermutation and class switch recombination are introduced by activation-induced cytidine deaminase (AID). AID is a highly mutagenic protein that is maintained in the cytoplasm at steady state, however AID is shuttled across the nuclear membrane and the protein transiently present in the nucleus appears sufficient for targeted alteration of immunoglobulin loci. AID has been implicated in epigenetic reprogramming in primordial germ cells and cell fusions and in induced pluripotent stem cells (iPS cells), however AID expression in non-B cells is very low. We hypothesised that epigenetic reprogramming would require a pathway that instigates prolonged nuclear residence of AID. Here we show that AID is completely re-localised to the nucleus during drug withdrawal following etoposide treatment, in the period in which double strand breaks (DSBs) are repaired. Re-localisation occurs 2-6 hours after etoposide treatment, and AID remains in the
A significant leap forward got here in 2000 with the invention that activation-induced deaminase (AID) is actually required for hypermutation. This used to be in 2002 by means of proof that reduction without delay edits the DNA that encodes an antibody in an activated B mobile. a lot has seeing that been learnt concerning the biochemistry and rules of reduction, however the mechanism during which it truly is recruited particularly to antibody-encoding genes continues to be enigmatic. figuring out this recruitment is clinically major simply because off-target relief job at oncogenes may end up in chromosomal translocations and tumorigenesis ...
Activation induced cytidine deaminase (AID) is required for somatic hypermutation (SHM) and class-switch recombination (CSR). AID initiates the processes that carry out immunoglobulin diversity by deaminating cytosine residues within variable (V) and switch (S) regions on the Ig locus during active transcription. The resulting G:U mispairs can then be replicated or repaired by cellular repair mechanisms to give rise to isotype-switched and antigen-specific mature antibodies.; In this study I have identified two novel phosphorylation sites, serine 41 and serine 43, and demonstrated their importance in AID activity as well as confirmed the importance of serine 38 phosphorylation. Phosphorylation null mutants generated by replacing serine with alanine are much less active than wild-type AID, as is non-phosphorylated AID purified from E. coli. In contrast, phosphorylation charge mimic mutants generated by replacing serine with aspartic acid, are (3-4) fold more active than wild-type AID. ...
Activation induced cytidine deaminase (AID) is required for somatic hypermutation (SHM) and class-switch recombination (CSR). AID initiates the processes that carry out immunoglobulin diversity by deaminating cytosine residues within variable (V) and switch (S) regions on the Ig locus during active transcription. The resulting G:U mispairs can then be replicated or repaired by cellular repair mechanisms to give rise to isotype-switched and antigen-specific mature antibodies.; In this study I have identified two novel phosphorylation sites, serine 41 and serine 43, and demonstrated their importance in AID activity as well as confirmed the importance of serine 38 phosphorylation. Phosphorylation null mutants generated by replacing serine with alanine are much less active than wild-type AID, as is non-phosphorylated AID purified from E. coli. In contrast, phosphorylation charge mimic mutants generated by replacing serine with aspartic acid, are (3-4) fold more active than wild-type AID. ...
However, we overlooked a mechanism natural has adopted for rapid evolution of proteins: adaptive immunity that generates a huge pool of antibodies.It is well-known that B-cells are capable of producing a large pool of new antibodies upon antigen stimuli, which is a most important protective mechanism for animals. People have been curious about the molecular mechanism of antibody generation. Recent works have revealed that an enzyme: Activation-Induced (Cytidine) Deaminase (AID) serves as an essential protein in three processes for antibody diversity, namely somatic hypermutation (SHM), class switch recombination (CSR) and gene conversion. Briefly speaking, AID converts cytidine to uracil by oxidizing the amino group to carbonyl group, resulting in mismatch of Watson-Crick base pair. Then DNA lesion repair pathways (base excision repair, BER; mismatch repair, MMR)are employed to bring DNA back to normal. In this process, the coding sequence for the hypervariable region of immunoglobulin is ...
Activation-induced cytidine deaminase (AICDA) antibody | Q9GZX7 | Activation-induced cytidine deaminase (AICDA), Cytidine aminohydrolase, AID
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Single-stranded DNA-specific cytidine deaminase. Involved in somatic hypermutation (SHM), gene conversion, and class-switch recombination (CSR) in B-lymphocytes by deaminating C to U during transcription of Ig-variable (V) and Ig-switch (S) region DNA. Required for several crucial steps of B-cell terminal differentiation necessary for efficient antibody responses. May also play a role in the epigenetic regulation of gene expression by participating in DNA demethylation.
The transcription factor STAT6 plays a key role in mediating signaling downstream of the receptors for IL-4 and IL-13. In B cells, STAT6 is required for class switch recombination to IgE and for germinal center formation during type 2 immune responses directed against allergens or helminths. In this study, we compared the transcriptomes and proteomes of primary mouse B cells from wild-type and STAT6-deficient mice cultured for 4 d in the presence or absence of IL-4. Microarray analysis revealed that 214 mRNAs were upregulated and 149 were downregulated ,3-fold by IL-4 in a STAT6-dependent manner. Across all samples, ∼5000 proteins were identified by label-free quantitative liquid chromatography/mass spectrometry. A total of 149 proteins was found to be differentially expressed ,3-fold between IL-4-stimulated wild-type and STAT6−/− B cells (75 upregulated and 74 downregulated). Comparative analysis of the proteome and transcriptome revealed that expression of these proteins was mainly ...
TY - JOUR. T1 - Doing more on the corporate sustainability front. T2 - A longitudinal analysis of csr reporting of global fashion companies. AU - Feng, Penglan. AU - Ngai, Cindy Sing bik. PY - 2020/3/1. Y1 - 2020/3/1. N2 - The fashion industry has been under the spotlight in recent years due to its negative social and environmental impacts. However, there is limited literature on how companies in the fashion industry communicate their corporate social responsibility (CSR) practices. This study aims to present a full picture of the paradigm of CSR reporting in the fashion industry by revealing the changes in CSR reporting practices and identifying the possible reasons behind the change. Content analysis was employed to investigate 12 global fashion companies 43 CSR reports from 2013 to 2016. Findings showed that more comprehensive CSR reporting was practiced in the fashion industry to meet stakeholders expectations. The reporting of 16 CSR issues experienced a rise. Labor and environmental ...
Concentration Unitmg/mLConcentration0.5Quantity0.1 mgVolume0.2ImmunogenLPS-activated CBA/Cs mouse splenic B cellsBackground InformationCD86 (B7-2) ...
CSR Europe offers its corporate members both issue-specific and benchmarking reports, which allow companies to better manage and integrate CSR strategies in their business structure.. Issue-specific reports provide in-depth analyses of topics relevant to a business corporate strategy. Through benchmarking reports, members may receive input on how to address a chosen area of their CSR strategy, based on both existing expertise and best practices from other companies.. In providing members with a framework of action for their own strategies and key topics, CSR Europe draws on its extensive work on all CSR issues and the database of methodologies and case-studies which its activities have generated.. For more information please contact Bernedine Bos.. ...
The Taft-Hartley Act made major changes to the Wagner Act. Although Section 7 was retained intact in the revised law, new language was added to provide that employees had the right to refrain from participating in union or mutual aid activities except that they could be required to become members in a union as a condition of employment.
India CSR News Network BHUBANESWAR: GMR Kamalanga Energy Limited (GKEL) organized three days training-cum-exposure program for farmers who have taken livestock.... ...
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The Bank has addressed this challenge through integrating corporate volunteering within its business practice and established clear principles and procedures for the implementation of volunteer activities in order to encourage its employees to participate and then initiate new actions... ...