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Anticorps
Numéro de catalogue:
(BOSSBS-12103R-A680)
Fournisseur:
Bioss
Description:
Glutamate receptors mediate most excitatory neurotransmission in the brain and play an important role in neural plasticity, neural development and neuro-degeneration. Ionotropic glutamate receptors are categorized into NMDA receptors and kainate/AMPA receptors, both of which contain glutamate-gated, cation-specific ion channels. Kainate/AMPA receptors co-localize with NMDA receptors in many synapses and consist of seven structurally related subunits designated GluR-1 to 7. The kainate/AMPA receptors are primarily responsible for fast excitatory neurotransmission by glutamate, whereas the NMDA receptors exhibit slow kinesis of Ca²⁺ ions and a high permeability for Ca²⁺ ions. One such NMDA receptor, NR3B, is expressed in motor neurons and forms cation channels impermeable to calcium, which can resist many open-channel blockers. NR3B functions in the brain as an excitatory glycine receptor, modifying the normal role of glycine as an inhibitory neurotransmitter.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-12103R-FITC)
Fournisseur:
Bioss
Description:
Glutamate receptors mediate most excitatory neurotransmission in the brain and play an important role in neural plasticity, neural development and neuro-degeneration. Ionotropic glutamate receptors are categorized into NMDA receptors and kainate/AMPA receptors, both of which contain glutamate-gated, cation-specific ion channels. Kainate/AMPA receptors co-localize with NMDA receptors in many synapses and consist of seven structurally related subunits designated GluR-1 to 7. The kainate/AMPA receptors are primarily responsible for fast excitatory neurotransmission by glutamate, whereas the NMDA receptors exhibit slow kinesis of Ca2+ ions and a high permeability for Ca2+ ions. One such NMDA receptor, NR3B, is expressed in motor neurons and forms cation channels impermeable to calcium, which can resist many open-channel blockers. NR3B functions in the brain as an excitatory glycine receptor, modifying the normal role of glycine as an inhibitory neurotransmitter.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-6515R-A350)
Fournisseur:
Bioss
Description:
C17orf71 belongs to the UPF0487 family. There are 3 isoforms produced by alternative splicing.Positive control;Human Anaplastic Thyroid Carcinoma, Human Breast Carcinoma.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-6515R-HRP)
Fournisseur:
Bioss
Description:
C17orf71 belongs to the UPF0487 family. There are 3 isoforms produced by alternative splicing.Positive control;Human Anaplastic Thyroid Carcinoma, Human Breast Carcinoma.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-13576R-CY5)
Fournisseur:
Bioss
Description:
ZBTB41/ZNF924
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-6515R-A750)
Fournisseur:
Bioss
Description:
C17orf71 belongs to the UPF0487 family. There are 3 isoforms produced by alternative splicing.Positive control;Human Anaplastic Thyroid Carcinoma, Human Breast Carcinoma.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-13575R-A680)
Fournisseur:
Bioss
Description:
Chromosome 1 is the largest human chromosome spanning about 260 million base pairs and making up 8% of the human genome. There are about 3,000 genes on chromosome 1, and considering the great number of genes there are also a large number of diseases associated with chromosome 1. Notably, the rare aging disease Hutchinson-Gilford progeria is associated with the LMNA gene which encodes lamin A. When defective, the LMNA gene product can build up in the nucleus and cause characteristic nuclear blebs. The mechanism of rapidly enhanced aging is unclear and is a topic of continuing exploration. The MUTYH gene is located on chromosome 1 and is partially responsible for familial adenomatous polyposis. Stickler syndrome, Parkinsons, Gaucher disease and Usher syndrome are also associated with chromosome 1. A breakpoint has been identified in 1q which disrupts the DISC1 gene and is linked to schizophrenia. Aberrations in chromosome 1 are found in a variety of cancers including head and neck cancer, malignant melanoma and multiple myeloma.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-0725R-CY7)
Fournisseur:
Bioss
Description:
Nuclear hormone receptor. The steroid hormones and their receptors are involved in the regulation of eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Ligand-dependent nuclear transactivation involves either direct homodimer binding to a palindromic estrogen response element (ERE) sequence or association with other DNA-binding transcription factors, such as AP-1/c-Jun, c-Fos, ATF-2, Sp1 and Sp3, to mediate ERE-independent signaling. Ligand binding induces a conformational change allowing subsequent or combinatorial association with multiprotein coactivator complexes through LXXLL motifs of their respective components. Mutual transrepression occurs between the estrogen receptor (ER) and NF-kappa-B in a cell-type specific manner. Decreases NF-kappa-B DNA-binding activity and inhibits NF-kappa-B-mediated transcription from the IL6 promoter and displace RELA/p65 and associated coregulators from the promoter. Recruited to the NF-kappa-B response element of the CCL2 and IL8 promoters and can displace CREBBP. Present with NF-kappa-B components RELA/p65 and NFKB1/p50 on ERE sequences. Can also act synergistically with NF-kappa-B to activate transcription involving respective recruitment adjacent response elements; the function involves CREBBP. Can activate the transcriptional activity of TFF1. Also mediates membrane-initiated estrogen signaling involving various kinase cascades. Essential for MTA1-mediated transcriptional regulation of BRCA1 and BCAS3 (By similarity).
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-6057R-A488)
Fournisseur:
Bioss
Description:
Distributive alpha-N-methyltransferase that methylates the N-terminus of target proteins containing the N-terminal motif [Ala/Pro/Ser]-Pro-Lys when the initiator Met is cleaved. Specifically catalyzes mono-, di- or tri-methylation of exposed alpha-amino group of Ala or Ser residue in the [Ala/Ser]-Pro-Lys motif and mono- or di-methylation of Pro in the Pro-Pro-Lys motif. Some of the substrates may be primed by METTL11B-mediated monomethylation. Responsible for the N-terminal methylation of KLHL31, MYL2, MYL3, RB1, RCC1, RPL23A and SET. Required during mitosis for normal bipolar spindle formation and chromosome segregation via its action on RCC1.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-6057R-A555)
Fournisseur:
Bioss
Description:
Distributive alpha-N-methyltransferase that methylates the N-terminus of target proteins containing the N-terminal motif [Ala/Pro/Ser]-Pro-Lys when the initiator Met is cleaved. Specifically catalyzes mono-, di- or tri-methylation of exposed alpha-amino group of Ala or Ser residue in the [Ala/Ser]-Pro-Lys motif and mono- or di-methylation of Pro in the Pro-Pro-Lys motif. Some of the substrates may be primed by METTL11B-mediated monomethylation. Responsible for the N-terminal methylation of KLHL31, MYL2, MYL3, RB1, RCC1, RPL23A and SET. Required during mitosis for normal bipolar spindle formation and chromosome segregation via its action on RCC1.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-0725R-CY5)
Fournisseur:
Bioss
Description:
Nuclear hormone receptor. The steroid hormones and their receptors are involved in the regulation of eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Ligand-dependent nuclear transactivation involves either direct homodimer binding to a palindromic estrogen response element (ERE) sequence or association with other DNA-binding transcription factors, such as AP-1/c-Jun, c-Fos, ATF-2, Sp1 and Sp3, to mediate ERE-independent signaling. Ligand binding induces a conformational change allowing subsequent or combinatorial association with multiprotein coactivator complexes through LXXLL motifs of their respective components. Mutual transrepression occurs between the estrogen receptor (ER) and NF-kappa-B in a cell-type specific manner. Decreases NF-kappa-B DNA-binding activity and inhibits NF-kappa-B-mediated transcription from the IL6 promoter and displace RELA/p65 and associated coregulators from the promoter. Recruited to the NF-kappa-B response element of the CCL2 and IL8 promoters and can displace CREBBP. Present with NF-kappa-B components RELA/p65 and NFKB1/p50 on ERE sequences. Can also act synergistically with NF-kappa-B to activate transcription involving respective recruitment adjacent response elements; the function involves CREBBP. Can activate the transcriptional activity of TFF1. Also mediates membrane-initiated estrogen signaling involving various kinase cascades. Essential for MTA1-mediated transcriptional regulation of BRCA1 and BCAS3 (By similarity).
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-0725R-FITC)
Fournisseur:
Bioss
Description:
Nuclear hormone receptor. The steroid hormones and their receptors are involved in the regulation of eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Ligand-dependent nuclear transactivation involves either direct homodimer binding to a palindromic estrogen response element (ERE) sequence or association with other DNA-binding transcription factors, such as AP-1/c-Jun, c-Fos, ATF-2, Sp1 and Sp3, to mediate ERE-independent signaling. Ligand binding induces a conformational change allowing subsequent or combinatorial association with multiprotein coactivator complexes through LXXLL motifs of their respective components. Mutual transrepression occurs between the estrogen receptor (ER) and NF-kappa-B in a cell-type specific manner. Decreases NF-kappa-B DNA-binding activity and inhibits NF-kappa-B-mediated transcription from the IL6 promoter and displace RELA/p65 and associated coregulators from the promoter. Recruited to the NF-kappa-B response element of the CCL2 and IL8 promoters and can displace CREBBP. Present with NF-kappa-B components RELA/p65 and NFKB1/p50 on ERE sequences. Can also act synergistically with NF-kappa-B to activate transcription involving respective recruitment adjacent response elements; the function involves CREBBP. Can activate the transcriptional activity of TFF1. Also mediates membrane-initiated estrogen signaling involving various kinase cascades. Essential for MTA1-mediated transcriptional regulation of BRCA1 and BCAS3 (By similarity).
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-0801R-CY5.5)
Fournisseur:
Bioss
Description:
Transmembrane serine/threonine kinase activin type-2 receptor forming an activin receptor complex with activin type-1 serine/threonine kinase receptors (ACVR1, ACVR1B or ACVR1c). Transduces the activin signal from the cell surface to the cytoplasm and is thus regulating many physiological and pathological processes including neuronal differentiation and neuronal survival, hair follicle development and cycling, FSH production by the pituitary gland, wound healing, extracellular matrix production, immunosuppression and carcinogenesis. Activin is also thought to have a paracrine or autocrine role in follicular development in the ovary. Within the receptor complex, the type-2 receptors act as a primary activin receptors (binds activin-A/INHBA, activin-B/INHBB as well as inhibin-A/INHA-INHBA). The type-1 receptors like ACVR1B act as downstream transducers of activin signals. Activin binds to type-2 receptor at the plasma membrane and activates its serine-threonine kinase. The activated receptor type-2 then phosphorylates and activates the type-1 receptor. Once activated, the type-1 receptor binds and phosphorylates the SMAD proteins SMAD2 and SMAD3, on serine residues of the C-terminal tail. Soon after their association with the activin receptor and subsequent phosphorylation, SMAD2 and SMAD3 are released into the cytoplasm where they interact with the common partner SMAD4. This SMAD complex translocates into the nucleus where it mediates activin-induced transcription. Inhibitory SMAD7, which is recruited to ACVR1B through FKBP1A, can prevent the association of SMAD2 and SMAD3 with the activin receptor complex, thereby blocking the activin signal. Activin signal transduction is also antagonized by the binding to the receptor of inhibin-B via the IGSF1 inhibin coreceptor (By similarity).
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-0725R-CY3)
Fournisseur:
Bioss
Description:
Nuclear hormone receptor. The steroid hormones and their receptors are involved in the regulation of eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Ligand-dependent nuclear transactivation involves either direct homodimer binding to a palindromic estrogen response element (ERE) sequence or association with other DNA-binding transcription factors, such as AP-1/c-Jun, c-Fos, ATF-2, Sp1 and Sp3, to mediate ERE-independent signaling. Ligand binding induces a conformational change allowing subsequent or combinatorial association with multiprotein coactivator complexes through LXXLL motifs of their respective components. Mutual transrepression occurs between the estrogen receptor (ER) and NF-kappa-B in a cell-type specific manner. Decreases NF-kappa-B DNA-binding activity and inhibits NF-kappa-B-mediated transcription from the IL6 promoter and displace RELA/p65 and associated coregulators from the promoter. Recruited to the NF-kappa-B response element of the CCL2 and IL8 promoters and can displace CREBBP. Present with NF-kappa-B components RELA/p65 and NFKB1/p50 on ERE sequences. Can also act synergistically with NF-kappa-B to activate transcription involving respective recruitment adjacent response elements; the function involves CREBBP. Can activate the transcriptional activity of TFF1. Also mediates membrane-initiated estrogen signaling involving various kinase cascades. Essential for MTA1-mediated transcriptional regulation of BRCA1 and BCAS3 (By similarity).
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-2219R-CY5)
Fournisseur:
Bioss
Description:
Pectinesterase inhibitor 18
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-2219R-CY5.5)
Fournisseur:
Bioss
Description:
Pectinesterase inhibitor 18
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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