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Anticorps
Numéro de catalogue:
(BOSSBS-1777R-A647)
Fournisseur:
Bioss
Description:
Receptor for gastrin and cholecystokinin. The CKK-B receptors occur throughout the central nervous system where they modulate anxiety, analgesia, arousal, and neuroleptic activity. This receptor mediates its action by association with G proteins that activate a phosphatidylinositol-calcium second messenger system. Isoform 2 is constitutively activated and may regulate cancer cell proliferation via a gastrin-independent mechanism.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-1777R-A488)
Fournisseur:
Bioss
Description:
Receptor for gastrin and cholecystokinin. The CKK-B receptors occur throughout the central nervous system where they modulate anxiety, analgesia, arousal, and neuroleptic activity. This receptor mediates its action by association with G proteins that activate a phosphatidylinositol-calcium second messenger system. Isoform 2 is constitutively activated and may regulate cancer cell proliferation via a gastrin-independent mechanism.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-4985R-CY5.5)
Fournisseur:
Bioss
Description:
Receptor tyrosine kinase which mediates actions of insulin-like growth factor 1 (IGF1). Binds IGF1 with high affinity and IGF2 and insulin (INS) with a lower affinity. The activated IGF1R is involved in cell growth and survival control. IGF1R is crucial for tumor transformation and survival of malignant cell. Ligand binding activates the receptor kinase, leading to receptor autophosphorylation, and tyrosines phosphorylation of multiple substrates, that function as signaling adapter proteins including, the insulin-receptor substrates (IRS1/2), Shc and 14-3-3 proteins. Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway and the Ras-MAPK pathway. The result of activating the MAPK pathway is increased cellular proliferation, whereas activating the PI3K pathway inhibits apoptosis and stimulates protein synthesis. Phosphorylated IRS1 can activate the 85 kDa regulatory subunit of PI3K (PIK3R1), leading to activation of several downstream substrates, including protein AKT/PKB. AKT phosphorylation, in turn, enhances protein synthesis through mTOR activation and triggers the antiapoptotic effects of IGFIR through phosphorylation and inactivation of BAD. In parallel to PI3K-driven signaling, recruitment of Grb2/SOS by phosphorylated IRS1 or Shc leads to recruitment of Ras and activation of the ras-MAPK pathway. In addition to these two main signaling pathways IGF1R signals also through the Janus kinase/signal transducer and activator of transcription pathway (JAK/STAT). Phosphorylation of JAK proteins can lead to phosphorylation/activation of signal transducers and activators of transcription (STAT) proteins. In particular activation of STAT3, may be essential for the transforming activity of IGF1R. The JAK/STAT pathway activates gene transcription and may be responsible for the transforming activity. JNK kinases can also be activated by the IGF1R.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-4985R-CY5)
Fournisseur:
Bioss
Description:
Receptor tyrosine kinase which mediates actions of insulin-like growth factor 1 (IGF1). Binds IGF1 with high affinity and IGF2 and insulin (INS) with a lower affinity. The activated IGF1R is involved in cell growth and survival control. IGF1R is crucial for tumor transformation and survival of malignant cell. Ligand binding activates the receptor kinase, leading to receptor autophosphorylation, and tyrosines phosphorylation of multiple substrates, that function as signaling adapter proteins including, the insulin-receptor substrates (IRS1/2), Shc and 14-3-3 proteins. Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway and the Ras-MAPK pathway. The result of activating the MAPK pathway is increased cellular proliferation, whereas activating the PI3K pathway inhibits apoptosis and stimulates protein synthesis. Phosphorylated IRS1 can activate the 85 kDa regulatory subunit of PI3K (PIK3R1), leading to activation of several downstream substrates, including protein AKT/PKB. AKT phosphorylation, in turn, enhances protein synthesis through mTOR activation and triggers the antiapoptotic effects of IGFIR through phosphorylation and inactivation of BAD. In parallel to PI3K-driven signaling, recruitment of Grb2/SOS by phosphorylated IRS1 or Shc leads to recruitment of Ras and activation of the ras-MAPK pathway. In addition to these two main signaling pathways IGF1R signals also through the Janus kinase/signal transducer and activator of transcription pathway (JAK/STAT). Phosphorylation of JAK proteins can lead to phosphorylation/activation of signal transducers and activators of transcription (STAT) proteins. In particular activation of STAT3, may be essential for the transforming activity of IGF1R. The JAK/STAT pathway activates gene transcription and may be responsible for the transforming activity. JNK kinases can also be activated by the IGF1R.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-6637R-A350)
Fournisseur:
Bioss
Description:
This gene has higher expression in p53-expressing cells than in control cells and is an immediate-early induction target of p53-mediated apoptosis. The protein encoded by this gene contains six putative transmembrane domains and may suppress cell growth by inducing apoptotic cell death through the caspase 9 and mitochondrial pathways. This gene is located on human chromosome 11q24, a region frequently altered in cancers. Alternative splicing results in two transcript variants encoding different isoforms. [provided by RefSeq, Jul 2008].
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-3502R-A647)
Fournisseur:
Bioss
Description:
Synapsin II is a member of the synapsin gene family. Synapsins are neuronal phosphoproteins which associate with the cytoplasmic surface of synaptic vesicles. Family members are characterized by common protein domains, and they are implicated in synaptogenesis and the modulation of neurotransmitter release, suggesting a potential role in several neuropsychiatric diseases. This member of the synapsin family is a neuron-specific phosphoprotein that selectively binds to small synaptic vesicles in the presynaptic nerve terminal.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-5353R-A647)
Fournisseur:
Bioss
Description:
FANCG, involved in Fanconi anemia, confers resistance to both hygromycin and mitomycin C. FANCG contains a 5-prime GC-rich untranslated region characteristic of housekeeping genes. The putative 622-amino acid protein has a leucine-zipper motif at its N-terminus. Fanconi anemia is an autosomal recessive disorder with diverse clinical symptoms, including developmental anomalies, bone marrow failure, and early occurrence of malignancies. A minimum of 8 FA genes have been identified.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-9178R-A680)
Fournisseur:
Bioss
Description:
X-linked recessive myotubular myopathy is a congenital muscular disease characterised by severe hypotonia and generalised muscle weakness that, in most cases, leads to early postnatal death. The gene responsible for myotubular myopathy MTM1 encodes a dual specificity phosphatase, named myotubularin, which is highly conserved through evolution. The gene for MTM1 is localised to a 300 kb critical region on human Xq128 between IDS and GRBRA3. Human MTM1, a 603 amino-acid protein, is mutated in myotubular myopathy. The largely related protein hMTMR2 is found mutated in a recessive form of Charcot-Marie-Tooth neuropathy. Myotubularin is primarily a lipid phosphatase that acts on phosphatidylinositol 3-monophosphate and is involved in the regulation of the phosphatidylinositol 3-kinase (PI3-kinase) pathway and membrane trafficking. Wild-type myotubularin can directly dephosphorylate PI3P and PI4P <i>in vitro</i>. Thus, it decreases PI3P levels by down-regulating PI3K activity and by facilitating the degradation of PI3P.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-9178R-A750)
Fournisseur:
Bioss
Description:
X-linked recessive myotubular myopathy is a congenital muscular disease characterised by severe hypotonia and generalised muscle weakness that, in most cases, leads to early postnatal death. The gene responsible for myotubular myopathy MTM1 encodes a dual specificity phosphatase, named myotubularin, which is highly conserved through evolution. The gene for MTM1 is localised to a 300 kb critical region on human Xq128 between IDS and GRBRA3. Human MTM1, a 603 amino-acid protein, is mutated in myotubular myopathy. The largely related protein hMTMR2 is found mutated in a recessive form of Charcot-Marie-Tooth neuropathy. Myotubularin is primarily a lipid phosphatase that acts on phosphatidylinositol 3-monophosphate and is involved in the regulation of the phosphatidylinositol 3-kinase (PI3-kinase) pathway and membrane trafficking. Wild-type myotubularin can directly dephosphorylate PI3P and PI4P <i>in vitro</i>. Thus, it decreases PI3P levels by down-regulating PI3K activity and by facilitating the degradation of PI3P.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-5353R-FITC)
Fournisseur:
Bioss
Description:
FANCG, involved in Fanconi anemia, confers resistance to both hygromycin and mitomycin C. FANCG contains a 5-prime GC-rich untranslated region characteristic of housekeeping genes. The putative 622-amino acid protein has a leucine-zipper motif at its N-terminus. Fanconi anemia is an autosomal recessive disorder with diverse clinical symptoms, including developmental anomalies, bone marrow failure, and early occurrence of malignancies. A minimum of 8 FA genes have been identified.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-11945R-HRP)
Fournisseur:
Bioss
Description:
Encoding over 1,100 genes within 132 million bases, chromosome 12 makes up about 4.5% of the human genome. A number of skeletal deformities are linked to chromosome 12 including hypochondrogenesis, achondrogenesis and Kniest dysplasia. Noonan syndrome, which includes heart and facial developmental defects among the primary symptoms, is caused by a mutant form of PTPN11 gene product, SH-PTP2. Chromosome 12 is also home to a homeobox gene cluster which encodes crucial transcription factors for morphogenesis, and the natural killer complex gene cluster encoding C-type lectin proteins which mediate the NK cell response to MHC I interaction. Trisomy 12p leads to facial development defects, seizure disorders and a host of other symptoms varying in severity depending on the extent of mosaicism and is most severe in cases of complete trisomy. The C12orf52 gene product has been provisionally designated C12orf52 pending further characterization.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-1502R-CY5)
Fournisseur:
Bioss
Description:
In addition to its role as a proinflammatory cytokine, may participate in T-cell effector function and perhaps T-cell development.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-1502R-CY5.5)
Fournisseur:
Bioss
Description:
In addition to its role as a proinflammatory cytokine, may participate in T-cell effector function and perhaps T-cell development.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-1495R-A350)
Fournisseur:
Bioss
Description:
May play a role in the formation and regulation of the tight junction (TJ) paracellular permeability barrier.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-7113R-CY7)
Fournisseur:
Bioss
Description:
Component of an E3 ubiquitin-protein ligase complex, in which it may act as a substrate recognition subunit. Involved in apoptosis by acting as a death receptor-associated protein that mediates apoptosis. Also involved in glucose homeostasis in pancreatic islet. Functions as an adapter/mediator in replication stress-induced signaling that leads to the activation of CHEK1.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-1065R-A555)
Fournisseur:
Bioss
Description:
May function as a regulator of the EGFR pathway. Probable tumor suppressor which may function in cell growth, proliferation and adhesion.
UOM:
1 * 100 µl
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