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block+heaters+
Numéro de catalogue:
(BOSSBS-5275R-FITC)
Fournisseur:
Bioss
Description:
Chk2 is a serine/threonine kinase involved in the control of cell cycle checkpoints, and may also participate in transduction of the DNA damage and replicational stress signals. Chk2 is the mammalian ortholog of the budding yeast Rad53 and fission yeast Cds1 checkpoint kinases. The amino-terminal domain of Chk2 contains a series of seven serine and threonine residues (Ser19, Thr26, Ser28, Ser33, Ser35, Ser50 and Thr68) followed by glutamine (SQ or TQ motif). These are known to be preferred sites for phosphorylation by ATM/ATR kinases. Indeed, after DNA damage by ionizing radiation (IR), UV irradiation or hydroxyurea treatment, Thr68 and other sites in this region become phosphorylated by ATM/ATR. The SQ/TQ cluster domain, therefore, seems to have a regulatory function. Phosphorylation at Thr68 is a prerequisite for the subsequent activation step, which is attributable to autophosphorylation of Chk2 on residues Thr383 and Thr387 in the activation loop of the kinase domain. Chk2 inhibits CDC25C phosphatase by phosphorylating it on Ser-216, preventing the entry into mitosis. This kinase may have a role in meiosis as well. Kinase activity is up regulated by autophosphorylation and the protein is rapidly phosphorylated in response to DNA damage and to replication block.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-5257R-HRP)
Fournisseur:
Bioss
Description:
Chk2 is a serine/threonine kinase involved in the control of cell cycle checkpoints, and may also participate in transduction of the DNA damage and replicational stress signals. Chk2 is the mammalian ortholog of the budding yeast Rad53 and fission yeast Cds1 checkpoint kinases. The amino-terminal domain of Chk2 contains a series of seven serine and threonine residues (Ser19, Thr26, Ser28, Ser33, Ser35, Ser50 and Thr68) followed by glutamine (SQ or TQ motif). These are known to be preferred sites for phosphorylation by ATM/ATR kinases. Indeed, after DNA damage by ionizing radiation (IR), UV irradiation or hydroxyurea treatment, Thr68 and other sites in this region become phosphorylated by ATM/ATR. The SQ/TQ cluster domain, therefore, seems to have a regulatory function. Phosphorylation at Thr68 is a prerequisite for the subsequent activation step, which is attributable to autophosphorylation of Chk2 on residues Thr383 and Thr387 in the activation loop of the kinase domain. Chk2 inhibits CDC25C phosphatase by phosphorylating it on Ser-216, preventing the entry into mitosis. This kinase may have a role in meiosis as well. Kinase activity is up regulated by autophosphorylation and the protein is rapidly phosphorylated in response to DNA damage and to replication block.
UOM:
1 * 100 µl
Fournisseur:
Thermo Fisher Scientific
Description:
En PP. Conviennent à tous les blocs de thermocycleurs de 0,2 ml et séquenceurs capillaires ABI PRISM® 310, 3100 et 3700. Disponible en blanc opaque pour procédures basées sur la luminescence.
Numéro de catalogue:
(BNUM1010-50)
Fournisseur:
Biotium
Description:
Cytochrome C is a well-characterized mobile electron transport protein that is essential to energy conversion in all aerobic organisms. In mammalian cells, this highly conserved protein is normally localized to the mitochondrial inter-membrane space. More recent studies have identified cytosolic cytochrome c as a factor necessary for activation of apoptosis. During apoptosis, cytochrome c is trans-located from the mitochondrial membrane to the cytosol, where it is required for activation of caspase-3 (CPP32). Overexpression of Bcl-2 has been shown to prevent the translocation of cytochrome c, thereby blocking the apoptotic process. Overexpression of Bax has been shown to induce the release of cytochrome c and to induce cell death. The release of cytochrome c from the mitochondria is thought to trigger an apoptotic cascade, whereby Apaf-1 binds to Apaf-3 (caspase-9) in a cytochrome c-dependent manner, leading to caspase-9 cleavage of caspase-3. This MAb recognizes total cytochrome C which includes both apocytochrome (i.e. cytochrome in the cytosol without heme attached) and holocytochrome (i.e cytochrome in the mitochondria with heme attached).
UOM:
1 * 50 µl
Fournisseur:
Biotium
Description:
This MAb reacts with a 28 kDa chain of HLA-DRB1 antigen, a member of MHC class II molecules. It does not cross react with HLA-DP and HLA-DQ. The L243 antibody recognizes a different epitope than the LN3 monoclonal antibody, and these antibodies do not cross-block binding to each other's respective epitopes. HLA-DR is a heterodimeric cell surface glycoprotein comprised of a 36 kDa alpha (heavy) chain and a 28 kDa beta (light) chain. It is expressed on B-cells, activated T-cells, monocytes/macrophages, dendritic cells and other non-professional APCs. In conjunction with the CD3/TCR complex and CD4 molecules, HLA-DR is critical for efficient peptide presentation to CD4 T cells. It is an excellent histiocytic marker in paraffin sections producing intense staining. True histiocytic neoplasms are similarly positive. HLA-DR antigens also occur on a variety of epithelial cells and their corresponding neoplastic counterparts. Loss of HLA-DR expression is related to tumor microenvironment and predicts adverse outcome in diffuse large B-cell lymphoma.
Fournisseur:
Biotium
Description:
This MAb reacts with a 28 kDa chain of HLA-DRB1 antigen, a member of MHC class II molecules. It does not cross react with HLA-DP and HLA-DQ. The L243 antibody recognizes a different epitope than the LN3 monoclonal antibody, and these antibodies do not cross-block binding to each other's respective epitopes. HLA-DR is a heterodimeric cell surface glycoprotein comprised of a 36 kDa alpha (heavy) chain and a 28 kDa beta (light) chain. It is expressed on B-cells, activated T-cells, monocytes/macrophages, dendritic cells and other non-professional APCs. In conjunction with the CD3/TCR complex and CD4 molecules, HLA-DR is critical for efficient peptide presentation to CD4 T cells. It is an excellent histiocytic marker in paraffin sections producing intense staining. True histiocytic neoplasms are similarly positive. HLA-DR antigens also occur on a variety of epithelial cells and their corresponding neoplastic counterparts. Loss of HLA-DR expression is related to tumor microenvironment and predicts adverse outcome in diffuse large B-cell lymphoma.
Numéro de catalogue:
(BOSSBS-12495R-A750)
Fournisseur:
Bioss
Description:
APOBEC proteins inhibit retroviruses by deaminating cytosine residues of viral RNA and DNA. The seven APOBEC3 genes or pseudogenes are found in a cluster thought to result from gene duplication on chromosome 22. Like APOBEC3G, APOBEC3F deaminates deoxycytosine to deoxyuracil in the minus strand of HIV-1 DNA, resulting in G to A hypermutation in the plus strand of DNA. Thus, APOBEC3G and APOBEC3F provide a mechanism for innate immunity to retroviruses, and are also likely contribute to sequence variation observed in many viruses. Viral infectivity factor (Vif) imparts APOBEC3G and APOBEC3F resistance to HIV through impaired translation of their mRNA and accelerated posttranslational degradation of the APOBEC3 proteins by the 26S proteasome. Interestingly, HIV-1 Vif cannot form a complex with APOBEC3G or APOBEC3F of mouse origin as it does with the human protein, and thus mouse APOBEC3G and APOBEC3F function as a potent inhibitors of wildtype HIV-1 replication, where human APOBEC3G and APOBEC3F are only able to inhibit Vif-deficient HIV-1 replication. This implies that induction of APOBEC3G and APOBEC3F activity or a method of blocking their interaction with Vif may provide a method for therapeutic intervention.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-12495R-A680)
Fournisseur:
Bioss
Description:
APOBEC proteins inhibit retroviruses by deaminating cytosine residues of viral RNA and DNA. The seven APOBEC3 genes or pseudogenes are found in a cluster thought to result from gene duplication on chromosome 22. Like APOBEC3G, APOBEC3F deaminates deoxycytosine to deoxyuracil in the minus strand of HIV-1 DNA, resulting in G to A hypermutation in the plus strand of DNA. Thus, APOBEC3G and APOBEC3F provide a mechanism for innate immunity to retroviruses, and are also likely contribute to sequence variation observed in many viruses. Viral infectivity factor (Vif) imparts APOBEC3G and APOBEC3F resistance to HIV through impaired translation of their mRNA and accelerated posttranslational degradation of the APOBEC3 proteins by the 26S proteasome. Interestingly, HIV-1 Vif cannot form a complex with APOBEC3G or APOBEC3F of mouse origin as it does with the human protein, and thus mouse APOBEC3G and APOBEC3F function as a potent inhibitors of wildtype HIV-1 replication, where human APOBEC3G and APOBEC3F are only able to inhibit Vif-deficient HIV-1 replication. This implies that induction of APOBEC3G and APOBEC3F activity or a method of blocking their interaction with Vif may provide a method for therapeutic intervention.
UOM:
1 * 100 µl
Numéro de catalogue:
(BNUM0057-50)
Fournisseur:
Biotium
Description:
This MAb reacts with a 28 kDa chain of HLA-DRB1 antigen, a member of MHC class II molecules. It does not cross react with HLA-DP and HLA-DQ. The L243 antibody recognizes a different epitope than the LN3 monoclonal antibody, and these antibodies do not cross-block binding to each other's respective epitopes. HLA-DR is a heterodimeric cell surface glycoprotein comprised of a 36 kDa alpha (heavy) chain and a 28 kDa beta (light) chain. It is expressed on B-cells, activated T-cells, monocytes/macrophages, dendritic cells and other non-professional APCs. In conjunction with the CD3/TCR complex and CD4 molecules, HLA-DR is critical for efficient peptide presentation to CD4 T cells. It is an excellent histiocytic marker in paraffin sections producing intense staining. True histiocytic neoplasms are similarly positive. HLA-DR antigens also occur on a variety of epithelial cells and their corresponding neoplastic counterparts. Loss of HLA-DR expression is related to tumor microenvironment and predicts adverse outcome in diffuse large B-cell lymphoma.
UOM:
1 * 50 µl
Numéro de catalogue:
(BOSSBS-12495R-A555)
Fournisseur:
Bioss
Description:
APOBEC proteins inhibit retroviruses by deaminating cytosine residues of viral RNA and DNA. The seven APOBEC3 genes or pseudogenes are found in a cluster thought to result from gene duplication on chromosome 22. Like APOBEC3G, APOBEC3F deaminates deoxycytosine to deoxyuracil in the minus strand of HIV-1 DNA, resulting in G to A hypermutation in the plus strand of DNA. Thus, APOBEC3G and APOBEC3F provide a mechanism for innate immunity to retroviruses, and are also likely contribute to sequence variation observed in many viruses. Viral infectivity factor (Vif) imparts APOBEC3G and APOBEC3F resistance to HIV through impaired translation of their mRNA and accelerated posttranslational degradation of the APOBEC3 proteins by the 26S proteasome. Interestingly, HIV-1 Vif cannot form a complex with APOBEC3G or APOBEC3F of mouse origin as it does with the human protein, and thus mouse APOBEC3G and APOBEC3F function as a potent inhibitors of wildtype HIV-1 replication, where human APOBEC3G and APOBEC3F are only able to inhibit Vif-deficient HIV-1 replication. This implies that induction of APOBEC3G and APOBEC3F activity or a method of blocking their interaction with Vif may provide a method for therapeutic intervention.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-4000R-A750)
Fournisseur:
Bioss
Description:
Chk2 is a serine/threonine kinase involved in the control of cell cycle checkpoints, and may also participate in transduction of the DNA damage and replicational stress signals. Chk2 is the mammalian ortholog of the budding yeast Rad53 and fission yeast Cds1 checkpoint kinases. The amino-terminal domain of Chk2 contains a series of seven serine and threonine residues (Ser19, Thr26, Ser28, Ser33, Ser35, Ser50 and Thr68) followed by glutamine (SQ or TQ motif). These are known to be preferred sites for phosphorylation by ATM/ATR kinases. Indeed, after DNA damage by ionizing radiation (IR), UV irradiation or hydroxyurea treatment, Thr68 and other sites in this region become phosphorylated by ATM/ATR. The SQ/TQ cluster domain, therefore, seems to have a regulatory function. Phosphorylation at Thr68 is a prerequisite for the subsequent activation step, which is attributable to autophosphorylation of Chk2 on residues Thr383 and Thr387 in the activation loop of the kinase domain. Chk2 inhibits CDC25C phosphatase by phosphorylating it on Ser-216, preventing the entry into mitosis. This kinase may have a role in meiosis as well. Kinase activity is up regulated by autophosphorylation and the protein is rapidly phosphorylated in response to DNA damage and to replication block.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-5275R-A488)
Fournisseur:
Bioss
Description:
Chk2 is a serine/threonine kinase involved in the control of cell cycle checkpoints, and may also participate in transduction of the DNA damage and replicational stress signals. Chk2 is the mammalian ortholog of the budding yeast Rad53 and fission yeast Cds1 checkpoint kinases. The amino-terminal domain of Chk2 contains a series of seven serine and threonine residues (Ser19, Thr26, Ser28, Ser33, Ser35, Ser50 and Thr68) followed by glutamine (SQ or TQ motif). These are known to be preferred sites for phosphorylation by ATM/ATR kinases. Indeed, after DNA damage by ionizing radiation (IR), UV irradiation or hydroxyurea treatment, Thr68 and other sites in this region become phosphorylated by ATM/ATR. The SQ/TQ cluster domain, therefore, seems to have a regulatory function. Phosphorylation at Thr68 is a prerequisite for the subsequent activation step, which is attributable to autophosphorylation of Chk2 on residues Thr383 and Thr387 in the activation loop of the kinase domain. Chk2 inhibits CDC25C phosphatase by phosphorylating it on Ser-216, preventing the entry into mitosis. This kinase may have a role in meiosis as well. Kinase activity is up regulated by autophosphorylation and the protein is rapidly phosphorylated in response to DNA damage and to replication block.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-5275R-A680)
Fournisseur:
Bioss
Description:
Chk2 is a serine/threonine kinase involved in the control of cell cycle checkpoints, and may also participate in transduction of the DNA damage and replicational stress signals. Chk2 is the mammalian ortholog of the budding yeast Rad53 and fission yeast Cds1 checkpoint kinases. The amino-terminal domain of Chk2 contains a series of seven serine and threonine residues (Ser19, Thr26, Ser28, Ser33, Ser35, Ser50 and Thr68) followed by glutamine (SQ or TQ motif). These are known to be preferred sites for phosphorylation by ATM/ATR kinases. Indeed, after DNA damage by ionizing radiation (IR), UV irradiation or hydroxyurea treatment, Thr68 and other sites in this region become phosphorylated by ATM/ATR. The SQ/TQ cluster domain, therefore, seems to have a regulatory function. Phosphorylation at Thr68 is a prerequisite for the subsequent activation step, which is attributable to autophosphorylation of Chk2 on residues Thr383 and Thr387 in the activation loop of the kinase domain. Chk2 inhibits CDC25C phosphatase by phosphorylating it on Ser-216, preventing the entry into mitosis. This kinase may have a role in meiosis as well. Kinase activity is up regulated by autophosphorylation and the protein is rapidly phosphorylated in response to DNA damage and to replication block.
UOM:
1 * 100 µl
Numéro de catalogue:
(BNUM0513-50)
Fournisseur:
Biotium
Description:
Recognizes a 53 kDa protein, which is identified as p53 suppressor gene product. It reacts with the mutant as well as the wild form of p53. Its epitope maps within the N-terminus (aa 37-45) of p53. Monoclonal antibody PAb1801 does not block the binding of DO-7 MAb to p53 in an ELISA test. p53 is a tumor suppressor gene expressed in a wide variety of tissue types and is involved in regulating cell growth, replication, and apoptosis. It binds to MDM2, SV40 T antigen and human papilloma virus E6 protein. Positive nuclear staining with p53 antibody has been reported to be a negative prognostic factor in breast carcinoma, lung carcinoma, colorectal, and urothelial carcinoma. Anti-p53 positivity has also been used to differentiate uterine serous carcinoma from endometrioid carcinoma as well as to detect intratubular germ cell neoplasia. Mutations involving p53 are found in a wide variety of malignant tumors, including breast, ovarian, bladder, colon, lung, and melanoma.
UOM:
1 * 50 µl
Numéro de catalogue:
(BOSSBS-7343R)
Fournisseur:
Bioss
Description:
CD265 is a member of the tumor necrosis factor receptor (TNFR) family. Human and murine CD265 share 81% amino acid identity in their extracellular domains. CD265 is widely expressed, with highest levels in skeletal muscle, thymus, liver, colon, small intestine and adrenal gland. CD265 is also expressed in dendritic cells. RANK and RANK ligand (RANKL) are important regulators of interactions between T cells and dendritic cells. RANK is the essential signaling receptor for osteoclast differentiation factor in osteoclastogenesis. Multiple tumor necrosis factor receptor-associated factors (TRAFs) are involved in the signaling of CD265. TRANCE (TNF-related activation-induced cytokines, also known as RANK ligand, osteoprotegerin ligand and osteoclast differentiation factor) is the ligand for CD265. The biological functions mediated by RANK include activation of NFkappaB and cjun N-terminal kinase, enhancement of T cell growth and dendritic cell function, induction of osteoclastogenesis and lymph node organogenesis. The soluble form of CD265 is able to block TRANCE induced biological activity. The binding of anti-CD265 to cell surface CD265 triggers signal transduction and induces CD265 mediated bioactivity.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-12495R-HRP)
Fournisseur:
Bioss
Description:
APOBEC proteins inhibit retroviruses by deaminating cytosine residues of viral RNA and DNA. The seven APOBEC3 genes or pseudogenes are found in a cluster thought to result from gene duplication on chromosome 22. Like APOBEC3G, APOBEC3F deaminates deoxycytosine to deoxyuracil in the minus strand of HIV-1 DNA, resulting in G to A hypermutation in the plus strand of DNA. Thus, APOBEC3G and APOBEC3F provide a mechanism for innate immunity to retroviruses, and are also likely contribute to sequence variation observed in many viruses. Viral infectivity factor (Vif) imparts APOBEC3G and APOBEC3F resistance to HIV through impaired translation of their mRNA and accelerated posttranslational degradation of the APOBEC3 proteins by the 26S proteasome. Interestingly, HIV-1 Vif cannot form a complex with APOBEC3G or APOBEC3F of mouse origin as it does with the human protein, and thus mouse APOBEC3G and APOBEC3F function as a potent inhibitors of wildtype HIV-1 replication, where human APOBEC3G and APOBEC3F are only able to inhibit Vif-deficient HIV-1 replication. This implies that induction of APOBEC3G and APOBEC3F activity or a method of blocking their interaction with Vif may provide a method for therapeutic intervention.
UOM:
1 * 100 µl
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est toujours affiché et vous avez besoin d'aide, s'il vous plaît appelez-nous au 016 385 011
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