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Bioss
Numéro de catalogue:
(BOSSBS-8338R-A750)
Fournisseur:
Bioss
Description:
Defects in PANK2 are the cause of neurodegeneration with brain iron accumulation type 1 (NBIA1); also known as pantothenate kinase-associated neurodegeneration (PKAN) or Hallervorden-Spatz syndrome (HSS). It is an autosomal recessive neurodegenerative disorder associated with iron accumulation in the brain, primarily in the basal ganglia. Clinical manifestations include progressive muscle spasticity, hyperreflexia, muscle rigidity, dystonia, dysarthria, and intellectual deterioration which progresses to severe dementia over several years. It is clinically classified into classic, atypical, and intermediate phenotypes. Classic forms present with onset in the first decade, rapid progression, loss of independent ambulation within 15 years. Atypical forms have onset in the second decade, slow progression, maintenance of independent ambulation up to 40 years later. Intermediate forms manifest onset in the first decade with slow progression or onset in the second decade with rapid progression. Patients with early onset tend to also develop pigmentary retinopathy, whereas those with later onset tend to also have speech disorders and psychiatric features. All patients have the 'eye of the tiger' sign on brain MRI.Defects in PANK2 are the cause of hypoprebetalipoproteinemia, acanthocytosis, retinitis pigmentosa, and pallidal degeneration (HARP). HARP is a rare syndrome with many clinical similarities to NBIA1.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-4169R-CY3)
Fournisseur:
Bioss
Description:
PTK9 is an actin-binding protein involved in motile and morphological processes. It inhibits actin polymerization, likely by sequestering G-actin. By capping the barbed ends of filaments, it also regulates motility. PTK9 seems to play an important role in clathrin-mediated endocytosis and distribution of endocytic organelles.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-8367R-CY5.5)
Fournisseur:
Bioss
Description:
Probable substrate-recognition component of a SCF-like ECS (Elongin-Cullin-SOCS-box protein) E3 ubiquitin ligase complex which mediates the ubiquitination and subsequent proteasomal degradation of target proteins.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-8367R-A555)
Fournisseur:
Bioss
Description:
Probable substrate-recognition component of a SCF-like ECS (Elongin-Cullin-SOCS-box protein) E3 ubiquitin ligase complex which mediates the ubiquitination and subsequent proteasomal degradation of target proteins.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-7725R-FITC)
Fournisseur:
Bioss
Description:
Component of cohesin complex, a complex required for the cohesion of sister chromatids after DNA replication. The cohesin complex apparently forms a large proteinaceous ring within which sister chromatids can be trapped. At anaphase, the complex is cleaved and dissociates from chromatin, allowing sister chromatids to segregate. The cohesin complex may also play a role in spindle pole assembly during mitosis.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-11337R-A555)
Fournisseur:
Bioss
Description:
C1q, a subcomponent of the classical complement pathway, is composed of nine subunits that mediate classical complement activation and thereby play an important role in the immune response. Six of these subunits are disulfide-linked dimers of chains A and B, while three of these subunits, designated C1q-A through C1q-C, are disulfide-linked dimers of chain C. The presence of receptors for C1q on effector cells modulates its activity, which may be antibody-dependent or independent. Macrophages are the primary source of C1q, while anti-inflammatory drugs as well as cytokines differentially regulate expression of the mRNA, as well as the protein. However, its ability to modulate the interaction of platelets with collagen and immune complexes suggests C1q influences homeostasis as well as other immune activities, and perhaps thrombotic complications resulting from immune injury. Defects in C1q-A, C1q-B and C1q-C cause inactivation of the classical pathway, leading to a rare genetic disorder characterized by lupus-like symptoms.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-11337R-A647)
Fournisseur:
Bioss
Description:
C1q, a subcomponent of the classical complement pathway, is composed of nine subunits that mediate classical complement activation and thereby play an important role in the immune response. Six of these subunits are disulfide-linked dimers of chains A and B, while three of these subunits, designated C1q-A through C1q-C, are disulfide-linked dimers of chain C. The presence of receptors for C1q on effector cells modulates its activity, which may be antibody-dependent or independent. Macrophages are the primary source of C1q, while anti-inflammatory drugs as well as cytokines differentially regulate expression of the mRNA, as well as the protein. However, its ability to modulate the interaction of platelets with collagen and immune complexes suggests C1q influences homeostasis as well as other immune activities, and perhaps thrombotic complications resulting from immune injury. Defects in C1q-A, C1q-B and C1q-C cause inactivation of the classical pathway, leading to a rare genetic disorder characterized by lupus-like symptoms.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-3834R-A350)
Fournisseur:
Bioss
Description:
MRPL12 is a component of the 39S subunit of mammalian mitochondrial ribosomes. This protein forms homodimers whereas in prokaryotic ribosomes two L7/L12 dimers and one L10 protein form the L8 protein complex.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-3559R-A488)
Fournisseur:
Bioss
Description:
mTOR controls cell growth, in part by regulating p70 S6 kinase alpha (p70alpha) and eukaryotic initiation factor 4E binding protein 1 (4EBP1). Raptor is a 150 kDa mTOR binding protein that also binds 4EBP1 and p70alpha. The binding of Raptor to mTOR is necessary for the mTOR-catalyzed phosphorylation of 4EBP1 in vitro, and it strongly enhances the mTOR kinase activity toward p70alpha. Rapamycin or amino acid withdrawal increases, whereas insulin strongly inhibits, the recovery of 4EBP1 and raptor on 7-methyl-GTP Sepharose. Partial inhibition of raptor expression by RNA interference (RNAi) reduces mTOR-catalyzed 4EBP1 phosphorylation in vitro. RNAi of C. elegans raptor yields an array of phenotypes that closely resemble those produced by inactivation of Ce-TOR. Thus, raptor is an essential scaffold for the mTOR-catalyzed phosphorylation of 4EBP1 and mediates TOR action in vivo.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-3559R-CY5.5)
Fournisseur:
Bioss
Description:
mTOR controls cell growth, in part by regulating p70 S6 kinase alpha (p70alpha) and eukaryotic initiation factor 4E binding protein 1 (4EBP1). Raptor is a 150 kDa mTOR binding protein that also binds 4EBP1 and p70alpha. The binding of Raptor to mTOR is necessary for the mTOR-catalyzed phosphorylation of 4EBP1 in vitro, and it strongly enhances the mTOR kinase activity toward p70alpha. Rapamycin or amino acid withdrawal increases, whereas insulin strongly inhibits, the recovery of 4EBP1 and raptor on 7-methyl-GTP Sepharose. Partial inhibition of raptor expression by RNA interference (RNAi) reduces mTOR-catalyzed 4EBP1 phosphorylation in vitro. RNAi of C. elegans raptor yields an array of phenotypes that closely resemble those produced by inactivation of Ce-TOR. Thus, raptor is an essential scaffold for the mTOR-catalyzed phosphorylation of 4EBP1 and mediates TOR action in vivo.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-7641R-A680)
Fournisseur:
Bioss
Description:
ACSM3.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-7641R-FITC)
Fournisseur:
Bioss
Description:
ACSM3
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-15352R-HRP)
Fournisseur:
Bioss
Description:
GPCR C5L2.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-3476R-CY5.5)
Fournisseur:
Bioss
Description:
YAP1 (also known as Yes associated protein 1) was originally identified as a transcription factor that binds to the SH3 domain of the YES kinase (a Src protein kinase). More recently it has been identified as a candidate oncogene that promotes tumorigenesis in many different types of cancer.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-11236R-A680)
Fournisseur:
Bioss
Description:
During vertebrate embryogenesis, a left right axis is established. Secreted growth factors of the TGF beta family, including gene products derived from nodal, lefty 1 and lefty 2, play crucial roles in establishing left right asymmetries. TGF beta (Transforming growth factor beta) is a pleiotropic cytokine that regulates growth and differentiation of diverse types of cells. TGF beta actions are directed by ligand induced activation of TGF beta receptors. Complexes formed move into the nucleus, where they act as components of a transcriptional complex. Lefty, a novel member of the TGF beta superfamily, inhibits TGF beta Signalling. Lefty acts to inhibit phosphorylation of Smad2 following activation of the TGF beta receptor. Lefty also inhibits events downstream from R Smad phosphorylation. Lefty provides a repressed state of TGF beta responsive genes. The Lefty family is comprised of Lefty 1 and Lefty 2 in mouse, and Lefty A and Lefty B in humans. Members of the TGF beta superfamily require processing for their activation. Cleavage is therefore an essential step for Lefty activation. Lefty is synthesised as a large inactive precursor (41 KDa) that must be endoproteolytically processed to release the bioactive polypeptide (28 kDa and 34 kDa forms). The 28kDa form induces MAPK activity.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-12086R-CY7)
Fournisseur:
Bioss
Description:
Associates with microtubules and may play a role in the microtubule-dependent transport of the GABA-B receptor. May play a role in JAK1 signaling and regulate microtubule cytoskeleton rearrangements.
UOM:
1 * 100 µl
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