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Fournisseur:  Bioss
Description:   2,4-Dichlorophenoxyacetic acid (2,4-D) is a common systemic herbicide used in the control of broadleaf weeds. It is the most widely used herbicide in the world, and the third most commonly used in North America. [1] 2,4-D is also an important synthetic auxin, often used in laboratories for plant research and as a supplement in plant cell culture media such as MS medium. 2,4-D is a synthetic auxin, which is a class of plant growth regulators. It is absorbed through the leaves and is translocated to the meristems of the plant. Uncontrolled, unsustainable growth ensues causing stem curl-over, leaf withering, and eventual plant death. 2,4-D is typically applied as an amine salt, but more potent ester versions exist as well.
UOM:  1 * 100 µl
Numéro de catalogue: (BOSSBS-11306R)

Fournisseur:  Bioss
Description:   Increase in fetal surfactant synthesis and lung maturity is caused by the glucocorticoidal induction of enzymes required for phosphatidylcholine synthesis towards the end of gestation (1). The regulation of gestational age-dependent induction of phosphatidylcholine synthesis by glucocorticoids is still unclear (1). The rate-controlling enzyme in the phosphatidylcholine biosynthetic pathway is CTP-phosphocholine cytidylyltransferase A (CCT A) (2–4). In cultured eukaryotic cells, this enzyme is essential for survival (3). The alpha isoform is located in the nucleus and is regulated by reversible phosphorylation and membrane association (3). There is significant identity between the alpha-helical membrane-binding domains of CCT A and soybean oleosin (2). Expressed CCT A has lipid-dependent cytidylyltransferase activity (5). The gene which encodes CCT A maps to human chromosome 3q (4).
UOM:  1 * 100 µl

Fournisseur:  Bioss
Description:   Increase in fetal surfactant synthesis and lung maturity is caused by the glucocorticoidal induction of enzymes required for phosphatidylcholine synthesis towards the end of gestation (1). The regulation of gestational age-dependent induction of phosphatidylcholine synthesis by glucocorticoids is still unclear (1). The rate-controlling enzyme in the phosphatidylcholine biosynthetic pathway is CTP-phosphocholine cytidylyltransferase A (CCT A) (2–4). In cultured eukaryotic cells, this enzyme is essential for survival (3). The alpha isoform is located in the nucleus and is regulated by reversible phosphorylation and membrane association (3). There is significant identity between the alpha-helical membrane-binding domains of CCT A and soybean oleosin (2). Expressed CCT A has lipid-dependent cytidylyltransferase activity (5). The gene which encodes CCT A maps to human chromosome 3q (4).
UOM:  1 * 100 µl
Numéro de catalogue: (BOSSBS-11306R-CY5)

Fournisseur:  Bioss
Description:   Increase in fetal surfactant synthesis and lung maturity is caused by the glucocorticoidal induction of enzymes required for phosphatidylcholine synthesis towards the end of gestation (1). The regulation of gestational age-dependent induction of phosphatidylcholine synthesis by glucocorticoids is still unclear (1). The rate-controlling enzyme in the phosphatidylcholine biosynthetic pathway is CTP-phosphocholine cytidylyltransferase A (CCT A) (2–4). In cultured eukaryotic cells, this enzyme is essential for survival (3). The alpha isoform is located in the nucleus and is regulated by reversible phosphorylation and membrane association (3). There is significant identity between the alpha-helical membrane-binding domains of CCT A and soybean oleosin (2). Expressed CCT A has lipid-dependent cytidylyltransferase activity (5). The gene which encodes CCT A maps to human chromosome 3q (4).
UOM:  1 * 100 µl

Fournisseur:  Biotium
Description:   This antibody neutralises HurTNFamediated cytotoxicity of L929 cells and inhibits tumour growth in mice. It protects mice against toxicity of HurTNFa. Tumor Necrosis Factor Alpha (TNF alpha) is a protein secreted by lipopolysaccharide-stimulated macrophages, and causes tumor necrosis when injected into tumor bearing mice. TNF alpha is believed to mediate pathogenic shock and tissue injury associated with endotoxemia. TNF alpha exists as a multimer of two, three, or five non-covalently linked units, but shows a single 17 kDa band following SDS PAGE under non-reducing conditions. TNF alpha is closely related to the 25 kDa protein Tumor Necrosis Factor beta (lymphotoxin), sharing the same receptors and cellular actions. TNF alpha causes cytolysis of certain transformed cells, being synergistic with interferon gamma in its cytotoxicity. Although it has little effect on many cultured normal human cells, TNF alpha appears to be directly toxic to vascular endothelial cells. Other actions of TNF alpha include stimulating growth of human fibroblasts and other cell lines, activating polymorphonuclear neutrophils and osteoclasts, and induction of interleukin 1, prostaglandin E2 and collagenase production.
UOM:  1 * 50 µl
Fournisseur:  Biotium
Description:   This antibody neutralises HurTNFamediated cytotoxicity of L929 cells and inhibits tumour growth in mice. It protects mice against toxicity of HurTNFa. Tumor Necrosis Factor Alpha (TNF alpha) is a protein secreted by lipopolysaccharide-stimulated macrophages, and causes tumor necrosis when injected into tumor bearing mice. TNF alpha is believed to mediate pathogenic shock and tissue injury associated with endotoxemia. TNF alpha exists as a multimer of two, three, or five non-covalently linked units, but shows a single 17 kDa band following SDS PAGE under non-reducing conditions. TNF alpha is closely related to the 25 kDa protein Tumor Necrosis Factor beta (lymphotoxin), sharing the same receptors and cellular actions. TNF alpha causes cytolysis of certain transformed cells, being synergistic with interferon gamma in its cytotoxicity. Although it has little effect on many cultured normal human cells, TNF alpha appears to be directly toxic to vascular endothelial cells. Other actions of TNF alpha include stimulating growth of human fibroblasts and other cell lines, activating polymorphonuclear neutrophils and osteoclasts, and induction of interleukin 1, prostaglandin E2 and collagenase production.
Fournisseur:  Biotium
Description:   This antibody neutralises HurTNFamediated cytotoxicity of L929 cells and inhibits tumour growth in mice. It protects mice against toxicity of HurTNFa. Tumor Necrosis Factor Alpha (TNF alpha) is a protein secreted by lipopolysaccharide-stimulated macrophages, and causes tumor necrosis when injected into tumor bearing mice. TNF alpha is believed to mediate pathogenic shock and tissue injury associated with endotoxemia. TNF alpha exists as a multimer of two, three, or five non-covalently linked units, but shows a single 17 kDa band following SDS PAGE under non-reducing conditions. TNF alpha is closely related to the 25 kDa protein Tumor Necrosis Factor beta (lymphotoxin), sharing the same receptors and cellular actions. TNF alpha causes cytolysis of certain transformed cells, being synergistic with interferon gamma in its cytotoxicity. Although it has little effect on many cultured normal human cells, TNF alpha appears to be directly toxic to vascular endothelial cells. Other actions of TNF alpha include stimulating growth of human fibroblasts and other cell lines, activating polymorphonuclear neutrophils and osteoclasts, and induction of interleukin 1, prostaglandin E2 and collagenase production.
Numéro de catalogue: (BOSSBS-1613R-A488)

Fournisseur:  Bioss
Description:   Vertebrate neuron-specific nuclear protein called NeuN (Neuronal Nuclei) is an excellent marker for neurons in primary cultures and in retinoic acid-stimulated P19 cells. It is also useful for identifying neurons in transplants. NeuN is a neuron-specific, DNA-binding nuclear protein in vertebrates. In mice, NeuN is observed in most neuronal cell types throughout the nervous system, including cerebellum, cerebral cortex, hippocampus, thalamus and spinal cord, as well as the dorsal root ganglia, sympathetic chain ganglia and enteric ganglia of the peripheral nervous system. NeuN immunoreactivity is first observed in neurons when they become post-mitotic and are initiating cellular and morphological differentiation. No staining is observed in proliferative zones. NeuN has been used as an immunohistochemical marker for excitotoxic lesions of the brain as well as in the diagnosis of a wide range of human tissue specimens from the central and peripheral nervous systems.
UOM:  1 * 100 µl

Fournisseur:  Biotium
Description:   This antibody neutralizes TNF alpha biological activities. It prevents TNF alpha induced apoptosis in Jurkat cells. It also neutralizes HurTNFamediated cytotoxicity of L929 cells and inhibits tumor growth in mice. It protects mice against toxicity of HurTNFa. Tumor Necrosis Factor Alpha (TNF alpha) is a protein secreted by lipopolysaccharide-stimulated macrophages, and causes tumor necrosis when injected into tumor bearing mice. TNF alpha is believed to mediate pathogenic shock and tissue injury associated with endotoxemia. TNF alpha exists as a multimer of two, three, or five non-covalently linked units, but shows a single 17 kDa band following SDS PAGE under non-reducing conditions. TNF alpha is closely related to the 25 kDa protein Tumor Necrosis Factor beta (lymphotoxin), sharing the same receptors and cellular actions. TNF alpha causes cytolysis of certain transformed cells, being synergistic with interferon gamma in its cytotoxicity. Although it has little effect on many cultured normal human cells, TNF alpha appears to be directly toxic to vascular endothelial cells. Other actions of TNF alpha include stimulating growth of human fibroblasts and other cell lines, activating polymorphonuclear neutrophils and osteoclasts, and induction of interleukin 1, prostaglandin E2 and collagenase production.
UOM:  1 * 50 µl
Fournisseur:  Biotium
Description:   This antibody neutralizes TNF alpha biological activities. It prevents TNF alpha induced apoptosis in Jurkat cells. It also neutralizes HurTNFamediated cytotoxicity of L929 cells and inhibits tumor growth in mice. It protects mice against toxicity of HurTNFa. Tumor Necrosis Factor Alpha (TNF alpha) is a protein secreted by lipopolysaccharide-stimulated macrophages, and causes tumor necrosis when injected into tumor bearing mice. TNF alpha is believed to mediate pathogenic shock and tissue injury associated with endotoxemia. TNF alpha exists as a multimer of two, three, or five non-covalently linked units, but shows a single 17 kDa band following SDS PAGE under non-reducing conditions. TNF alpha is closely related to the 25 kDa protein Tumor Necrosis Factor beta (lymphotoxin), sharing the same receptors and cellular actions. TNF alpha causes cytolysis of certain transformed cells, being synergistic with interferon gamma in its cytotoxicity. Although it has little effect on many cultured normal human cells, TNF alpha appears to be directly toxic to vascular endothelial cells. Other actions of TNF alpha include stimulating growth of human fibroblasts and other cell lines, activating polymorphonuclear neutrophils and osteoclasts, and induction of interleukin 1, prostaglandin E2 and collagenase production.
Numéro de catalogue: (BSENC-1377-50)

Fournisseur:  Biosensis
Description:   Neurofilaments can be defined as the intermediate or 10nm diameter filaments found in neuronal cells. They are composed a mixture of subunits which often includes the neurofilament triplet proteins, NF-L, NF-M and NF-H. Neurofilaments may also include peripherin, alpha-internexin, nestin and in some cases vimentin. Alpha-internexin is a ~66 kDa Class IV intermediate filament subunit expressed in large amounts early in neuronal development, but is downregulated in many neurons as development procedes. Many classes of mature neurons contain alpha-internexin in addition to NF-L, NF-M and NF-H. In some mature neurons alpha-internexin is the only neurofilament subunit expressed. Antibodies to alpha-internexin are therefore unique probes to study and classify neuronal types and follow their processes in sections and in tissue culture. In addition the very early developmental expression of alpha-internexin means its presence is an early and convenient diagnostic feature of neuronal progenitors cells and other cell committed to the neuronal lineage.
UOM:  1 * 50 µl
Numéro de catalogue: (BOSSBS-13006R)

Fournisseur:  Bioss
Description:   Ubiquitin-like protein modifier which can be covalently attached to target protein and subsequently leads to their degradation by the 26S proteasome, in a NUB1L-dependent manner. Probably functions as a survival factor. Conjugation ability activated by UBA6. Promotes the expression of the proteasome subunit beta type-9 (PSMB9/LMP2). Regulates TNF-alpha-induced and LPS-mediated activation of the central mediator of innate immunity NF-kappa-B by promoting TNF-alpha-mediated proteasomal degradation of ubiquitinated-I-kappa-B-alpha. Required for TNF-alpha-induced p65 nuclear translocation in renal tubular epithelial cells (RTECs). May be involved in dendritic cell (DC) maturation, the process by which immature dendritic cells differentiate into fully competent antigen-presenting cells that initiate T-cell responses. Mediates mitotic non-disjunction and chromosome instability, in long-term in vitro culture and cancers, by abbreviating mitotic phase and impairing the kinetochore localization of MAD2L1 during the prometaphase stage of the cell cycle. May be involved in the formation of aggresomes when proteasome is saturated or impaired. Mediates apoptosis in a caspase-dependent manner, especially in renal epithelium and tubular cells during renal diseases such as polycystic kidney disease and Human immunodeficiency virus (HIV)-associated nephropathy (HIVAN).
UOM:  1 * 100 µl
Fournisseur:  Thermo Fisher Scientific
Description:   En PP avec capuchon fileté en PP et zone inscriptible, stériles. Pour le stockage cryogénique des cultures cellulaires, des cultures microbiologiques ou d’autres spécimens. Bonnes performances dans les congélateurs mécaniques et dans l’azote liquide (phase gazeuse et liquide*).
Numéro de catalogue: (BOSSBS-11027R-A680)

Fournisseur:  Bioss
Description:   NKHC1 is a neuronal-specific component of a multi-subunit molecular motor complex that mediates intracellular organelle transport. Mutations in the gene encoding NKHC1 cause autosomal dominant spastic paraplegia 10. NKHC1 has a pan-neuronal distribution in the nervous system. Rat tissue extracts by immunoblot of NKHC1 can produce a doublet only in brain and sciatic nerve tissue. NKHC1 is distributed throughout the central nervous system and is enriched in subsets of neurons. Within cultured hippocampal neurons, NKHC1 is concentrated in the perinuclear region of the cell body. Kinesin superfamily proteins like NKHC1 are the molecular motors conveying cargos along microtubules.
UOM:  1 * 100 µl
Fournisseur:  Cytiva (Formerly Pall Lab)
Description:   The Pall AcroPrep™ Advance 96-well long tip filter plate for nucleic acid binding (NAB) incorporates a silica-based quartz glass fibre media to allow for efficient binding of DNA and RNA, while providing smooth flow and rapid processing of samples. This media offers researchers the flexibility to purify plasmid DNA from bacteria, and genomic DNA or total RNA from cell culture samples using a single plate.
UOM:  1 * 5 ST
Numéro de catalogue: (BOSSBS-11308R)

Fournisseur:  Bioss
Description:   Steroid 5a-Reductase is an important enzyme in androgen physiology because it catalyzes the conversion of testosterone into the more potent 5a-dihydro-testosterone, which mediates androgen effects on target tissues. The enzyme exists as two isoforms: type 1, which is expressed mainly in the skin; and type 2, which is expressed mainly in the prostate. In cultured human skin cells, 5a-Reductase 1 shows heterogeneity of protein, and has different levels of transcriptional and translational expression. 5a-Reductase 1 is expressed in all portions of the hair follicle, whereas 5a-Reductase 2 is expressed only in mesenchymal portions. In addition, 5a-Reductase 1 is mainly expressed in human breast carcinoma and may play a role in the in situ production and actions of the potent androgen 5a-dihydrotestosterone, including inhibition of cancer cell proliferation in hormone-dependent human breast carcinoma. The 5a-Reductase-3a-hydroxysteroid dehydrogenase complex is present in the human brain, suggesting that the complex may be involved in the synthesis of neuroactive steroids or the catabolism of neurotoxic steroids.
UOM:  1 * 100 µl
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