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Anticorps
Numéro de catalogue:
(USBI043253-AP)
Fournisseur:
US Biological
Description:
Anti-TRIM58 Rabbit Polyclonal Antibody (AP (Alkaline Phosphatase))
UOM:
1 * 200 µl
Numéro de catalogue:
(BOSSBS-3703R-A647)
Fournisseur:
Bioss
Description:
Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; the function is largely independent of transcription. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seem to have to effect on cell-cycle regulation. Implicated in Notch signaling cross-over. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Isoform 2 enhances the transactivation activity of isoform 1 from some but not all TP53-inducible promoters. Isoform 4 suppresses transactivation activity and impairs growth suppression mediated by isoform 1. Isoform 7 inhibits isoform 1-mediated apoptosis.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-6730R-A555)
Fournisseur:
Bioss
Description:
Functions as a transcriptional activator in a promoter context-dependent manner. Modulates the placental expression of CYP11A1. Involved in regulation of the alpha-globin gene in erythroid cells. Activation of the alpha-globin promoter in erythroid cells is via synergistic interaction with TFCP2 (By similarity). Involved in regulation of the alpha-globin gene in erythroid cells. Binds strongly to sequences around the HIV-1 initiation site and weakly over the TATA-box. Represses HIV-1 transcription by inhibiting the binding of TFIID to the TATA-box.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-2901R-A488)
Fournisseur:
Bioss
Description:
Negatively regulates matrix metalloproteinase-9 (MMP-9) by suppressing MMP-9 secretion and by direct inhibition of its enzymatic activity. RECK down-regulation by oncogenic signals may facilitate tumor invasion and metastasis. Appears to also regulate MMP-2 and MT1-MMP, which are involved in cancer progression.
UOM:
1 * 100 µl
Numéro de catalogue:
(USBIA0004-11H)
Fournisseur:
US Biological
Description:
Anti-ABCG1 Rabbit Polyclonal Antibody (HRP (Horseradish Peroxidase))
UOM:
1 * 100 µl
Numéro de catalogue:
(USBIA0004-02K1)
Fournisseur:
US Biological
Description:
Anti-ABCA1 Rat Monoclonal Antibody (PE (Phycoerythrin)) [clone: 10B15]
UOM:
1 * 1 EA
Numéro de catalogue:
(USBIA0000-33D-FITC)
Fournisseur:
US Biological
Description:
Anti-GPA33 Rabbit Polyclonal Antibody (FITC (Fluorescein Isothiocyanate))
UOM:
1 * 200 µl
Numéro de catalogue:
(USBIT0850-02)
Fournisseur:
US Biological
Description:
Anti-Tamm-Horsfall Glycoprotein Sheep Polyclonal Antibody
UOM:
1 * 1 mL
Numéro de catalogue:
(BOSSBS-1817R-CY5)
Fournisseur:
Bioss
Description:
Direct ligand for ERBB3 and ERBB4 tyrosine kinase receptors. Concomitantly recruits ERBB1 and ERBB2 coreceptors, resulting in ligand-stimulated tyrosine phosphorylation and activation of the ERBB receptors. The multiple isoforms perform diverse functions such as inducing growth and differentiation of epithelial, glial, neuronal, and skeletal muscle cells; inducing expression of acetylcholine receptor in synaptic vesicles during the formation of the neuromuscular junction; stimulating lobuloalveolar budding and milk production in the mammary gland and inducing differentiation of mammary tumor cells; stimulating Schwann cell proliferation; implication in the development of the myocardium such as trabeculation of the developing heart. Isoform 10 may play a role in motor and sensory neuron development.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-8257R-HRP)
Fournisseur:
Bioss
Description:
Probable transcriptional regulator involved in developmental processes. Is required for normal development of the pharyngeal arch arteries.Involvement in disease:Haploinsufficiency of the TBX1 gene is responsible for most of the physical malformations present in DiGeorge syndrome (DGS) and velocardiofacial syndrome (VCFS) . DGS is characterized by the association of several malformations: hypoplastic thymus and parathyroid glands, congenital conotruncal cardiopathy, and a subtle but characteristic facial dysmorphology. VCFS is marked by the association of congenital conotruncal heart defects, cleft palate or velar insufficiency, facial dysmorpholgy and learning difficulties. It is now accepted that these two syndromes represent two forms of clinical expression of the same entity manifesting at different stages of life.Defects in TBX1 are a cause of DiGeorge syndrome (DGS) .Defects in TBX1 are a cause of velocardiofacial syndrome (VCFS) .Defects in TBX1 are a cause of conotruncal heart malformations (CTHM). CTHM consist of cardiac outflow tract defects, such as tetralogy of Fallot, pulmonary atresia, double-outlet right ventricle, truncus arteriosus communis, and aortic arch anomalies.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-8257R-FITC)
Fournisseur:
Bioss
Description:
Probable transcriptional regulator involved in developmental processes. Is required for normal development of the pharyngeal arch arteries.Involvement in disease:Haploinsufficiency of the TBX1 gene is responsible for most of the physical malformations present in DiGeorge syndrome (DGS) and velocardiofacial syndrome (VCFS) . DGS is characterized by the association of several malformations: hypoplastic thymus and parathyroid glands, congenital conotruncal cardiopathy, and a subtle but characteristic facial dysmorphology. VCFS is marked by the association of congenital conotruncal heart defects, cleft palate or velar insufficiency, facial dysmorpholgy and learning difficulties. It is now accepted that these two syndromes represent two forms of clinical expression of the same entity manifesting at different stages of life.Defects in TBX1 are a cause of DiGeorge syndrome (DGS) .Defects in TBX1 are a cause of velocardiofacial syndrome (VCFS) .Defects in TBX1 are a cause of conotruncal heart malformations (CTHM). CTHM consist of cardiac outflow tract defects, such as tetralogy of Fallot, pulmonary atresia, double-outlet right ventricle, truncus arteriosus communis, and aortic arch anomalies.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-4511R-CY5.5)
Fournisseur:
Bioss
Description:
Tubulin is the major constituent of microtubules. It binds two moles of GTP, one at an exchangeable site on the beta chain and one at a non-exchangeable site on the alpha chain.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-8259R-A488)
Fournisseur:
Bioss
Description:
Catalyzes the NAD-dependent oxidative cleavage of spermidine and the subsequent transfer of the butylamine moiety of spermidine to the epsilon-amino group of a specific lysine residue of the eIF-5A precursor protein to form the intermediate deoxyhypusine residue.
UOM:
1 * 100 µl
Fournisseur:
Biotium
Description:
The family of EF-hand type Ca2 -binding proteins includes calbindin, S-100 alpha and beta, calgranulins, B and C, and the parvalbumin family members, including parvalbumin alpha and parvalbumin beta. The S-100 protein is involved in the regulation of cellular processes such as cell cycle progression and differentiation. S-100 protein may function in the activation of Ca2 induced Ca2 release, inhibition of microtubule assembly and inhibition of protein kinase C mediated phosphorylation. Two S-100 subunits, sharing 60% sequence identity, have been described as S-100 alpha chain and S-100 beta chain. Three S-100 dimeric forms have been characterized, differing in their subunit composition of two alpha chains, two beta chains or one alpha and one beta chain. S-100 localizes to the cytoplasm and nuclei of astrocytes, Schwann s cells, ependymomas and astrogliomas. S-100 is also detected in almost all benign naevi, malignant melanocytic tumours and in Langerhans cells in the skin. Calbindin, S-100 proteins and parvalbumin proteins are each expressed in neural tissues. In addition, S-100 alpha and beta are present in a variety of other tissues and calbindin is present in intestine and kidney.
Fournisseur:
Biotium
Description:
This MAb reacts with both SUMO-2 and SUMO-3. The small ubiquitin-related modifier (SUMO) proteins, which include SUMO-1, 2 and 3, belong to the ubiquitin-like protein family. Like ubiquitin, the SUMO proteins are synthesized as precursor proteins that undergo processing before conjugation to target proteins. Also, both utilize the E1, E2 and E3 cascade enzymes for conjugation. However, SUMO and ubiquitin differ with respect to targeting. Ubiquitination predominantly targets proteins for degradation, whereas sumoylation targets proteins to a variety of cellular processing, including nuclear transport, transcriptional regulation, apoptosis and protein stability. The unconjugated SUMO-1, 2 and 3 proteins localize to the nuclear membrane, nuclear bodies and cytoplasm, respectively. SUMO-1 utilizes Ubc9 for conjugation to several target proteins, which include MDM2, p53, PML and RanGap1. SUMO-2 and 3 contribute to a greater percentage of protein modification than does SUMO-1 and unlike SUMO-1, they can form polymeric chains. In addition, SUMO-3 regulates beta-Amyloid generation and may be critical in the onset or progression of Alzheimer’s disease.
Numéro de catalogue:
(BOSSBS-13267R-FITC)
Fournisseur:
Bioss
Description:
GALK2 is important in the first step of the galactose metabolism pathway. GALK1, which belongs to the GHMP kinase family of proteins, is a crucial enzyme for galactose metabolism, specifically converting ?d-galactose to galactose 1-phosphate. Defects in the gene encoding GALK1 can cause galactosemia II, an autosomal recessive disorder characterized by congenital cataracts during infancy, often within the first two weeks of life. In the adult population, galactosemia II can cause presenile cataracts that are secondary to accumulation of galactitol in the lens of the eye. A second gene, GALK2, encodes an enzyme with greater activity against GalNAc than galactose. GALK2 has been implicated in the salvage pathway for the reutilization of free GalNAc derived from the degradation of complex carbohydrates.
UOM:
1 * 100 µl
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