Proteolysis of the class II-associated invariant chain generates a peptide binding site in intracellular HLA-DR molecules. Proc. Natl. Acad. Sci. USA. 1991. 88:
RefSeq Summary (NM_002118): HLA-DMB belongs to the HLA class II beta chain paralogues. This class II molecule is a heterodimer consisting of an alpha (DMA) and a beta (DMB) chain, both anchored in the membrane. It is located in intracellular vesicles. DM plays a central role in the peptide loading of MHC class II molecules by helping to release the CLIP (class II-associated invariant chain peptide) molecule from the peptide binding site. Class II molecules are expressed in antigen presenting cells (APC: B lymphocytes, dendritic cells, macrophages). The beta chain is approximately 26-28 kDa and its gene contains 6 exons. Exon one encodes the leader peptide, exons 2 and 3 encode the two extracellular domains, exon 4 encodes the transmembrane domain and exon 5 encodes the cytoplasmic tail. [provided by RefSeq, Jul 2008]. Publication Note: This RefSeq record includes a subset of the publications that are available for this gene. Please see the Gene record to access additional publications. ...
AE37 peptide/GM-CSF vaccine: A vaccine containing HER2/Neu-derived epitope (amino acids 776-790) linked to li-Key peptide (li-Key/HER2/neu hybrid peptide or AE37), and combined with granulocyte-macrophage colony-stimulating factor (GM-CSF), with potential antineoplastic and immunoadjuvant activities. Upon vaccination, AE37 may activate the immune system and stimulate T-helper cells against HER2/Neu expressing cancer cells. GM-CSF may potentiate the immune response against cancer cells expressing the HER2/Neu antigen. The Ii-Key moiety, a 4-amino acid (LRMK) epitope from the MHC class II-associated invariant chain (Ii protein), increases T-helper cell stimulation against HER2/neu antigen when compared to unmodified class II epitopes. HER2/neu, a tumor associated antigen (TAA), is overexpressed in a variety of tumor cell types and is highly immunogenic. Check for active clinical trials or closed clinical trials using this agent. (NCI Thesaurus) -- from cancer.gov ...
Improved risk models of patients with stage III melanoma will improve the treatment of patients with this disease; however, molecular markers are lacking. Our analysis of independent cohorts (two for protein in TMA, and one for mRNA in TCGA) of patients tumors strongly implicates increased CD74 expression as a new marker of good prognosis in stage III melanoma. Previously, we had considered inflammatory markers to be associated with poor prognosis, which was the case for MIF in both cohorts, and for iNOS in the MDACC cohort. The surprising finding of higher expression of CD74 having a strong association with good prognosis is most intriguing, and elucidating the mechanism involved is likely to open new avenues for melanoma research.. The functional role of CD74 is not well understood. Historically, CD74 was known primarily as the MHC class II invariant chain and functions in the molecular processing of MHC II through the Golgi (24). It has a potential role in the antitumor immune response (25), ...
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Clone REA296 recognizes MHC class II-associated invariant chain (Ii)-derived peptide (CLIP) complexes. MHC class II αβ heterodimers associate early during biosynthesis with a type II membrane protein, the invariant chain (Ii). The invariant chain serves as a chaperone for MHC II molecules and mediates trafficking to the endosomal pathway. In the endosomal pathway Ii is sequentially degraded, leaving a residual CLIP in the peptide-binding groove of MHC II. In presence of antigen peptide fragments, HLA-DM then binds to the MHC II molecule, releasing CLIP and allowing peptides to bind. REA296 detects HLA class II-positive cells which have impaired HLA-DM activity, and tumor cells that have escaped immuno-surveillance by CD4-positive T cells.Additional information: Clone REA296 displays negligible binding to Fc receptors. - Belgique
TY - JOUR. T1 - Structural Analysis of Invariant Chain Subsets as a Function of Their Association with MHC Class II Chains. AU - Nguyen, Q. V.. AU - Reyes, Victor. AU - Humphreys, R. E.. PY - 1995/2/20. Y1 - 1995/2/20. N2 - Respective subsets of human invariant chain (Ii), as identified with antibodies to two different epitopes, were characterized as a function of their associations with major histocompatibility complex (MHC) class II α,β chains and intracellular processing. E1 antiserum to Ii(183-193) and VIC-Y1 monoclonal antibody to an N-terminal determinant identified Ii(E1) and Ii(VIC) populations, respectively. Ii proteins comprise several species which have been defined with either genomic or post-translational processes: Ii itself; IpN and IpO, which represent the glycosylated forms on asparagine or threonine/serine, respectively; γ2 and γ3, which originate from an alternative initiation site for transcription; and p41, which has a 64-amino-acid insert which originated from an ...
The spatiotemporal regulation of the immune response remains largely unknown. Now Faure-André et al. (see the Perspective by Lukacs-Kornek and Turley) show that the invariant chain, a key regulator of antigen processing and presentation by major histocompatibility complex (MHC) class II molecules, also controls the intrinsic migratory capacity of dendritic cells. In a study of the behavior of dendritic cells taken from mouse models on microfabricated surfaces using time-lapse imaging, the invariant chain caused dendritic cells to enter a discontinuous migration mode that alternated between low- and high-motility phases. This regulation of dendritic cell migration by the invariant chain results from its association with the actin-based motor protein, myosin II. This use of common regulators for antigen processing and cell motility may provide dendritic cells with a way to coordinate the two functions in time and space.. G. Faure-André, P. Vargas, M.-I. Yuseff, M. Heuzé, J. Diaz, D. Lankar, V. ...
The goal of the Phase I part of this clinical research study is to find the highest tolerable dose of milatuzumab that can be given to patients with NHL or CLL. The goal of the Phase II part of this clinical research study is to learn if milatuzumab can help to control NHL or CLL. The safety of the study drug will also be studied.
Milatuzumab or placebo will be given subcutaneously once weekly for 4 weeks to determine if milatuzumab helps to control lupus (SLE). The treatment portion of the study lasts 4 weeks. Then patients are followed for disease activity for at least 12 weeks. If patients respond to the study drug, they may be eligible for one course of retreatment, again followed by 12 weeks of follow-up. Patients who showed a response will continue to be followed at timepoints up to one year after treatment to assess how long the response lasts ...
Milatuzumab or placebo will be given subcutaneously once weekly for 4 weeks to determine if milatuzumab helps to control lupus (SLE). The treatment portion of the study lasts 4 weeks. Then patients are followed for disease activity for at least 12 weeks. If patients respond to the study drug, they may be eligible for one course of retreatment, again followed by 12 weeks of follow-up. Patients who showed a response will continue to be followed at timepoints up to one year after treatment to assess how long the response lasts ...
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CD74, the cell-surface form of the MHC class II invariant chain, is a key inflammatory factor that is involved in various immune-mediated diseases as part of the macrophage migration inhibitory factor (MIF) binding complex. However, little is known about the natural regulators of CD74 in this context. In order to study the role of the HLA-DR molecule in regulating CD74, we used the HLA-DRα1 domain, which was shown to bind to and downregulate CD74 on CD11b+ monocytes. We found that DRα1 directly inhibited binding of MIF to CD74 and blocked its downstream inflammatory effects in the spinal cord of mice with experimental autoimmune encephalomyelitis (EAE). Potency of the DRα1 domain could be destroyed by trypsin digestion but enhanced by addition of a peptide extension (myelin oligodendrocyte glycoprotein [MOG]-35-55 peptide) that provided secondary structure not present in DRα1. These data suggest a conformationally sensitive determinant on DRα1-MOG that is responsible for optimal binding to ...
B cell maturation starts in the bone marrow but is completed in the spleen (Hardy et al., 2007). Survival of IgM+ splenic B cells is linked to the antiapoptotic B cell lymphoma 2 (BCL2) family of proteins and their opposing proapoptotic antagonist, BCL2-interacting mediator of cell death (BIM; Enders et al., 2003), and depends on tonic signals from surface IgM and IgD B cell antigen receptors transmitted through spleen tyrosine kinase (SYK), Brutons tyrosine kinase (BTK), and phosphatidylinositol 3 kinase (Srinivasan et al., 2009). Starting from the transitional 2 (T2) stage, B cells also depend on survival signals provided by a circulating cytokine, B cell-activating factor (BAFF), engaging the BAFF receptor (BAFFR; Khan, 2009). BCRs and BAFFR signal via pathways that activate transcription factors of the NF-κB family, and these play essential roles in mediating survival of B cells (Siebenlist et al., 2005).. CD74, also called MHC II invariant chain or Ii, is a type 2 transmembrane protein ...
B cell maturation starts in the bone marrow but is completed in the spleen (Hardy et al., 2007). Survival of IgM+ splenic B cells is linked to the antiapoptotic B cell lymphoma 2 (BCL2) family of proteins and their opposing proapoptotic antagonist, BCL2-interacting mediator of cell death (BIM; Enders et al., 2003), and depends on tonic signals from surface IgM and IgD B cell antigen receptors transmitted through spleen tyrosine kinase (SYK), Brutons tyrosine kinase (BTK), and phosphatidylinositol 3 kinase (Srinivasan et al., 2009). Starting from the transitional 2 (T2) stage, B cells also depend on survival signals provided by a circulating cytokine, B cell-activating factor (BAFF), engaging the BAFF receptor (BAFFR; Khan, 2009). BCRs and BAFFR signal via pathways that activate transcription factors of the NF-κB family, and these play essential roles in mediating survival of B cells (Siebenlist et al., 2005).. CD74, also called MHC II invariant chain or Ii, is a type 2 transmembrane protein ...
The invariant chain (Ii) binds nascent major histocompatibility complex (MHC) class II molecules, blocking peptide binding until the complex dissociates in the endosomes. This may serve to differentiate the MHC class I and II antigen presentation pathways and enable class II molecules to efficiently bind peptides in the endosomes. This hypothesis was addressed by probing spleen cells from a combination of knock-out and transgenic mice with a large panel of T cell hybridomas. The Ii molecule blocked the presentation of a range of endogenously synthesized epitopes, but some epitopes actually required Ii. Thus, the influence of Ii on presentation does not follow simple rules. In addition, mice expressing Ii were not tolerant to epitopes unmasked in its absence, a finding with possible implications for autoimmunity. ...
Males from the BXSB murine strain (H-2b) spontaneously develop an autoimmune syndrome with features of systemic lupus erythematosus (SLE), which results in part from the action of a mutant gene (Yaa) located on the Y chromosome. Like other H-2b mice, the BXSB strain does not express the class II major histocompatibility complex antigen, I-E. Here we report that the expression of I-E (E alpha dE beta b) in BXSB males bearing an E alpha d transgene prevents hypergammaglobulinemia, autoantibody production, and subsequent autoimmune glomerulonephritis. These transgenic mice bear on the majority of their B cells not only I-E molecules, but also an I-E alpha chain-derived peptide presented by a higher number of I-Ab molecules, as recognized by the Y-Ae monoclonal antibody. The I-E+ B cells appear less activated in vivo than the I-E- B cells, a minor population. This limited activation of the I-E+ B cells does not reflect a functional deficiency of this cell population, since it can be stimulated to ...
Mouse anti-CD23/Fc epsilon RII, Clone: EBVCS2, Cy5.5, PerCP, Novus Biologicals 100 Tests; Cy5.5, PerCP Life Sciences:Antibodies:Primary Antibodies:Flow Cytometry (Flow)
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Professional antigen-presenting cells secrete major histocompatibility complex class II (MHC II) carrying exosomes with unclear physiological function(s). Exosomes are first generated as the intraluminal vesicles (ILVs) of a specific type of multivesicular body, and are then secreted by fusion of th …
Helper T cells are stimulated to fight infections or diseases upon recognition of peptides from antigens that are processed and presented by the proteins of Major Histocompatibility Complex (MHC) Class II molecules. Degradation of a full protein into small peptide fragments is a lengthy process consisting of many steps and chaperones. Malfunctions during any step of antigen processing could lead to the development of self-reactive T cells or defective immune response to pathogens. Although much has been accomplished regarding how antigens are processed and presented to T cells, many questions still remain unanswered, preventing the design of therapeutics for direct intervention with antigen processing. Here, we review published work on the discovery and function of a MHC class II molecular chaperone, HLA-DO, in human, and its mouse analog H2-O, herein called DO. While DO was originally discovered decades ago, elucidating its function has proven challenging. DO was discovered in association with
Milatuzumab (or hLL1) is an anti-CD74 humanized monoclonal antibody for the treatment of multiple myeloma non-Hodgkins lymphoma and chronic lymphocytic leukemia. The drug is the first anti-CD74 antibody that has entered into human testing and is currently being studied for the treatment of multiple myeloma. Milatuzumab has received orphan drug designation from the Food and Drug Administration in the United States for the treatment of multiple myeloma and chronic lymphocytic leukemia. Milatuzumab was developed by Immunomedics, Inc, (Morris Plains NJ USA). CD74 is present on a variety of hematological tumors and even on some solid cancers. It is present in limited amounts in normal tissues but widely found in leukemias, lymphomas and the vast majority of multiple myeloma cases.[citation needed] CD74 is involved in a cell-to-cell communication pathway that is critical for survival.[citation needed] When CD74 is blocked by milatuzumab, it can lead to cell death. CD74 is an attractive target for a ...
The endocytic pathway comprises various organelles of low pH, including early endosomes, late endosomes and lysosomes, each with varying capacities for protein degradation and protein recycling. Certain proteins, such as transferrin receptors, are sorted for retrieval from endocytic compartments and are selectively recycled back to the PM or TGN, whereas those that are targeted for degradation are retained in late endosomes and lysosomes ( Piper and Katzmann, 2007). Upon reaching the late endosomes, proteins that are intended for destruction are sorted onto intraluminal vesicles that are derived from the inward budding of the limiting membrane of the endosome, thereby giving rise to multivesicular antigen-processing compartments termed multivesicular bodies (MVBs). The endosomal sorting complex required for transport (ESCRT) protein machinery, either directly through the recognition of the small molecule ubiquitin or indirectly through ubiquitin-independent targeting, sorts molecules that are ...
MO-DC generated in vitro serve as a model type of DC to unravel the complex interactions among DC maturation, MHC class II peptide loading, and endocytic transport (3, 33, 34). The emerging picture suggests that endocytic protease activity is regulated by differential activity of the lysosomal ATPase during DC maturation (3). By analyzing lysosomal MBP processing at pH 5.0 in vitro, we have here mimicked the conditions present in the lysosomal compartment of DC in the activated state in vivo.. The MHC class II-associated proteolytic machinery is characterized by a hierarchical proteolytic cascade, where the initial step controls the efficiency of Ag processing, peptide presentation, and T cell activation (14). Different types of APC as well as primary cells and immortalized cell lines contain distinct activity patterns of endocytic proteases (11, 17, 31, 35, 36, 37) which might result in different processing pathways for a given Ag and hence in different selections of peptides presented. We here ...
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RefSeq Summary (NM_006120): HLA-DMA belongs to the HLA class II alpha chain paralogues. This class II molecule is a heterodimer consisting of an alpha (DMA) and a beta chain (DMB), both anchored in the membrane. It is located in intracellular vesicles. DM plays a central role in the peptide loading of MHC class II molecules by helping to release the CLIP molecule from the peptide binding site. Class II molecules are expressed in antigen presenting cells (APC: B lymphocytes, dendritic cells, macrophages). The alpha chain is approximately 33-35 kDa and its gene contains 5 exons. Exon one encodes the leader peptide, exons 2 and 3 encode the two extracellular domains, exon 4 encodes the transmembrane domain and the cytoplasmic tail. [provided by RefSeq, Jul 2008]. Publication Note: This RefSeq record includes a subset of the publications that are available for this gene. Please see the Gene record to access additional publications. ##Evidence-Data-START## Transcript exon combination :: BC011447.1, ...
De Novo drug design aims at predicting the peptide leads for anti-malarial activity from the designed set of 200 templates (Dipeptide, tripeptide, tet..
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Hi, I am super new to HF and I am trying to perform a simple linear probing using CLIP as a baseline. I see some tutorials to add a classification layer for BERT but I dont see any for CLIP so I was wondering if theres…
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The ability of the immune system to eliminate and shape the immunogenicity of tumours defines the process of cancer immunoediting1. Immunotherapies such as those that target immune checkpoint molecules can be used to augment immune-mediated elimination of tumours and have resulted in durable responses in patients with cancer that did not respond to previous treatments. However, only a subset of patients benefit from immunotherapy and more knowledge about what is required for successful treatment is needed2-4. Although the role of tumour neoantigen-specific CD8+ T cells in tumour rejection is well established5-9, the roles of other subsets of T cells have received less attention. Here we show that spontaneous and immunotherapy-induced anti-tumour responses require the activity of both tumour-antigen-specific CD8+ and CD4+ T cells, even in tumours that do not express major histocompatibility complex (MHC) class II molecules. In addition, the expression of MHC class II-restricted antigens by tumour cells
My major interest is in antigen processing, defined as the combination of mechanisms that generate the complexes of class I and class II MHC molecules with peptides that are the targets for recognition by T lymphocytes. My colleagues and I have identified a number of proteins that collaborate in these processes. MHC class I peptide binding occurs in the context of a large complex that we have defined in the endoplasmic reticulum consisting of TAP, an ATP-dependent peptide transporter; tapasin, a protein that couples the transporter to assembling class I molecules; and two house-keeping chaperones, calreticulin and ERp57. How these accessory molecules combine to facilitate peptide binding is currently being intensively investigated. We have also studied MHC class II peptide binding through the mechanism of class II molecules being delivered into the endocytic pathway by an associated protein, the invariant chain. This has included study of the CLIP, a residual fragment of the invariant chain, ...
Has a strict specificity for hydrolysis of asparaginyl bonds. Can also cleave aspartyl bonds slowly, especially under acidic conditions. May be involved in the processing of proteins for MHC class II antigen presentation in the lysosomal/endosomal system. Required for normal lysosomal protein degradation in renal proximal tubules. Required for normal degradation of internalized EGFR. Plays a role in the regulation of cell proliferation via its role in EGFR degradation.
TY - JOUR. T1 - Val-tyr, an Angiotensin I Converting Enzyme Inhibitor from Sardines that have Resistance to Gastrointestinal Proteases. AU - Seki, Eiji. AU - Osajima, Katsuhiro. AU - Matsufuji, Hiroshi. AU - Matsui, Toshiro. AU - Osajima, Yutaka. PY - 1995/1/1. Y1 - 1995/1/1. N2 - The NH2-terminal residue of a dipeptide is an important determinant of the resistance to peptidases of porcine small mucosa. NH2-terminal Val or Ile, and COOH-terminal Trp or Tyr dipeptides had higher angiotensin I converting enzyme(ACE)inhibitory activity and digestive resistance than other dipeptides. We defined Val-Tyr as a main inhibitor in alkaline protease hydrolyzates from sardines. Attempts to isolate and measurement of Val-Tyr were done from the short chain peptides that reduced blood pressure. The content of Val-Tyr was 51 mg per 100 g of the short chain peptides, represented 1.3% of the total ACE inhibitory activity of the short chain peptides. Isolated Val-Tyr was resistant to gastrointestinal proteases. ...
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HLA class II histocompatibility antigen gamma chain also known as HLA-DR antigens-associated invariant chain or CD74 (Cluster of Differentiation 74), is a protein that in humans is encoded by the CD74 gene. The invariant chain (Abbreviated Ii) is a polypeptide involved in the formation and transport of MHC class II protein. The cell surface form of the invariant chain is known as CD74. The nascent MHC class II protein in the rough ER binds a segment of the invariant chain (Ii; a trimer) in order to shape the peptide binding groove and prevent formation of a closed conformation. Binding to Ii might also prevent binding of peptides from the endogenous pathway to the groove of MHC class II. The invariant chain also facilitates MHC class IIs export from the ER in a vesicle. The signal for endosomal targeting resides in the cytoplasmic tail of the invariant chain. This fuses with a late endosome containing the endocytosed proteins. It is then cleaved by cathepsin S (cathepsin L in cortical thymic ...
Over the last decade, our understanding and ability to predict the MHC class I pathway antigen presentation has improved substantially. This however does not hold for post-transnationally modified (PTM) antigens, where our understanding on how PTMs impact the potential for antigen presentation remains limited. Likewise, is our ability to predict MHC class II antigen presentation limited, and data suggest that properties other that MHC binding plays a critical role for the prediction of CD4 epitopes. Finally, is our understanding of the role of the T cell and the similarity of the presented peptide to the self proteome in the context of peptide immunogenicity very limited ...
|p|One of the first cytokines described, MIF (macrophage migration inhibitory factor) was originally identified in studies of delayed hypersensitivity reactions where it was shown to inhibit macrophage migration. It is an important mediator of the innate immune response with potential roles in the pathophysiology of inflammatory, autoimmune, and neoplastic disorders. The human MIF gene encodes a 115 amino acid, 12.5 kDa secreted protein. Crystallographic studies suggest that MIF exists as a homotrimer, although some reports show that it may exist as a dimer or monomer as well. Although MIF exhibits no homology with other known cytokines, it shares structural homology with several bacterial enzymes. It has been speculated that MIF is an inflammatory mediator possibly associated with rheumatoid arthritis (RA) severity.|/p|
Macrophage migration inhibitory factor (MIF) is an evolutionary conserved 12.5-kDa protein mediator with multiple functions in innate and acquired immunity. Upon leaderless secretion, MIF acts as a typical inflammatory cytokine, but there is no structural homology between MIF and any of the known cy …
In article ,01bc8736$e36ebb80$0b0b258a at rhgf001,, N. Sheikh ,rhgf001 at mailrelay.qmw.ac.uk, wrote: ,Hi, ,I am trying to block the class II antigen processing pathway in mice - has ,anyone tried this ? , ,I am thinking of using Chloroquine - does anybody have any ideas on doses ? I dont know if anyone has done much with this - it seems kind of tricky to do systemically. For one thing, the proteases thought to be involved in Class II processing are probably important in other cellular functions, especially normal cellular protein turnover. FWIW, chloroquine concs. of 100-200 micromolar are sufficient to block most processing in vitro, but I dont know what effect that might have on the viability of non-presenting cells. ,Or are there any alternatives - even knockout mice...which are defective in ,class II processing ? Aside from the Class II knockouts, there are two that might be useful. Both invariant chain and H-2M knockouts have presentation defects, although neither stems from problems ...
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Macrophage migration inhibitory factor (MIF), a proinflammatory cytokine, is considered an attractive therapeutic target in multiple inflammatory and autoimmune disorders. In addition to its known biologic activities, MIF can also function as a tautomerase. Several small molecules have been reported to be effective inhibitors of MIF tautomerase activity in vitro. Herein we employed a robust activity-based assay to identify different classes of novel inhibitors of the catalytic and biological activities of MIF. Several novel chemical classes of inhibitors of the catalytic activity of MIF with IC(50) values in the range of 0.2-15.5 microm were identified and validated. The interaction site and mechanism of action of these inhibitors were defined using structure-activity studies and a battery of biochemical and biophysical methods. MIF inhibitors emerging from these studies could be divided into three categories based on their mechanism of action: 1) molecules that covalently modify the catalytic site at
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The nascent MHC class II protein in the rough ER has its peptide-binding cleft blocked by the invariant chain (Ii; a trimer) to prevent it from binding cellular peptides or peptides from the endogenous pathway. The invariant chain also facilitates MHC class IIs export from the ER in a vesicle. This fuses with a late endosome containing the endocytosed, degraded proteins. It is then broken down in stages, leaving only a small fragment called CLIP which still blocks the peptide binding cleft. An MHC class II-like structure, HLA-DM, removes CLIP and replaces it with a peptide from the endosome. The stable MHC class-II is then presented on the cell surface ...
The B cell surface molecule B1 is functionally linked with B cell activation and differentiation. J Immunol. 1985 Aug; 135(2):973-9 ...
Y. Mizue, S. Ghani, L. Leng, C. McDonald, P. Kong, J. Baugh, S. J. Lane, J. Craft, J. Nishihira, S. C. Donnelly, Z. Zhu, R. Bucala ...
Swanson B.J., Jaeck H.-M., Lyons G.E. (1998). Characterization of myocyte enhancer factor 2 (MEF2) expression in B and T cells: MEF2C is a B cell-restricted transcription factor in lymphocytes.. Mol. Immunol. 35: 445 - 458. PubMed DOI:10.1016/S0161-5890(98)00058-3 ...
Has strong elastinolytic activity, even at neutral pH, and may play a role in tissue damage associated with inflammation (Kirschke et al., 1989; Shi et al., 1992). Facilitates antigen presentation in the MHC class II system by degradation of the invariant chain (Driessen et al., 1999), and may therefore by a target for attenuation of immune response ...