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cell+culture+flasks
Numéro de catalogue:
(BOSSBS-1335R-CY5)
Fournisseur:
Bioss
Description:
Functions as a receptor for membrane-bound ligands Jagged1, Jagged2 and Delta1 to regulate cell-fate determination. Upon ligand activation through the released notch intracellular domain (NICD) it forms a transcriptional activator complex with RBPJ/RBPSUH and activates genes of the enhancer of split locus. Affects the implementation of differentiation, proliferation and apoptotic programs. Involved in angiogenesis; negatively regulates endothelial cell proliferation and migration and angiogenic sprouting. Involved in the maturation of both CD4+ and CD8+ cells in the thymus. Important for follicular differentiation and possibly cell fate selection within the follicle. During cerebellar development, functions as a receptor for neuronal DNER and is involved in the differentiation of Bergmann glia. Represses neuronal and myogenic differentiation. May play an essential role in postimplantation development, probably in some aspect of cell specification and/or differentiation. May be involved in mesoderm development, somite formation and neurogenesis. May enhance HIF1A function by sequestering HIF1AN away from HIF1A. Required for the THBS4 function in regulating protective astrogenesis from the subventricular zone (SVZ) niche after injury. Involved in determination of left/right symmetry by modulating the balance between motile and immotile (sensory) cilia at the left-right organiser (LRO).
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-3705R-CY3)
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-3705R-CY7)
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-3703R-CY7)
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
Fournisseur:
ENZO LIFE SCIENCES
Description:
Mdivi-1 is a selective inhibitor of mitochondrial division in yeast and mammalian cells which acts via inhibiting the mitochondrial division dynamin. In cells, Mdivi-1 inhibits apoptosis by inhibiting mitochondrial outer membrane permeabilization. Mdivi-1 causes the rapid (50= ~10µM. In yeast, time-lapse fluorescence microscopy revealed no detectable mitochondrial division after treatment with Mdivi-1. It inhibits Dnm1 GTPase activity in a dose dependent manner with an estimated IC50 of 1-10µM but is not a general inhibitor of GTPases.
Numéro de catalogue:
(BOSSBS-12577R-A647)
Fournisseur:
Bioss
Description:
BCL2 is an integral outer mitochondrial membrane protein that blocks the apoptotic death of some cells such as lymphocytes. Constitutive expression of BCL2, such as in the case of translocation of BCL2 to Ig heavy chain locus, is thought to be the cause of follicular lymphoma. Two transcript variants (alpha and beta) produced by alternate splicing, differ in their C-terminal ends. BCL2 suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. It regulates cell death by controlling the mitochondrial membrane permeability. It appears to function in a feedback loop system with caspases. BCL2 inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF1). It can form homodimers, and heterodimers with BAX, BAD, BAK and BclX(L). Heterodimerization with BAX requires intact BH1 and BH2 domains, and is necessary for anti-apoptotic activity. Also interacts with APAF1, RAF1, TP53BP2, BBC3, BCL2L1 and BNIPL.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-12577R-FITC)
Fournisseur:
Bioss
Description:
BCL2 is an integral outer mitochondrial membrane protein that blocks the apoptotic death of some cells such as lymphocytes. Constitutive expression of BCL2, such as in the case of translocation of BCL2 to Ig heavy chain locus, is thought to be the cause of follicular lymphoma. Two transcript variants (alpha and beta) produced by alternate splicing, differ in their C-terminal ends. BCL2 suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. It regulates cell death by controlling the mitochondrial membrane permeability. It appears to function in a feedback loop system with caspases. BCL2 inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF1). It can form homodimers, and heterodimers with BAX, BAD, BAK and BclX(L). Heterodimerization with BAX requires intact BH1 and BH2 domains, and is necessary for anti-apoptotic activity. Also interacts with APAF1, RAF1, TP53BP2, BBC3, BCL2L1 and BNIPL.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-12577R-HRP)
Fournisseur:
Bioss
Description:
BCL2 is an integral outer mitochondrial membrane protein that blocks the apoptotic death of some cells such as lymphocytes. Constitutive expression of BCL2, such as in the case of translocation of BCL2 to Ig heavy chain locus, is thought to be the cause of follicular lymphoma. Two transcript variants (alpha and beta) produced by alternate splicing, differ in their C-terminal ends. BCL2 suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. It regulates cell death by controlling the mitochondrial membrane permeability. It appears to function in a feedback loop system with caspases. BCL2 inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF1). It can form homodimers, and heterodimers with BAX, BAD, BAK and BclX(L). Heterodimerization with BAX requires intact BH1 and BH2 domains, and is necessary for anti-apoptotic activity. Also interacts with APAF1, RAF1, TP53BP2, BBC3, BCL2L1 and BNIPL.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-12577R-A488)
Fournisseur:
Bioss
Description:
BCL2 is an integral outer mitochondrial membrane protein that blocks the apoptotic death of some cells such as lymphocytes. Constitutive expression of BCL2, such as in the case of translocation of BCL2 to Ig heavy chain locus, is thought to be the cause of follicular lymphoma. Two transcript variants (alpha and beta) produced by alternate splicing, differ in their C-terminal ends. BCL2 suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. It regulates cell death by controlling the mitochondrial membrane permeability. It appears to function in a feedback loop system with caspases. BCL2 inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF1). It can form homodimers, and heterodimers with BAX, BAD, BAK and BclX(L). Heterodimerization with BAX requires intact BH1 and BH2 domains, and is necessary for anti-apoptotic activity. Also interacts with APAF1, RAF1, TP53BP2, BBC3, BCL2L1 and BNIPL.
UOM:
1 * 100 µl
Fournisseur:
Shenandoah Biotechnology
Description:
Platelet-derived growth factor (PDGF) is an important regulator of cell growth, proliferation, and angiogenesis. PDGF synthesis is induced by IL-1, IL-6, TNF-α, TGF-β, and EGF signaling. PDGF functions as a mitogenic growth hormone on cells of mesenchymal lineage, such as smooth muscle and glial cells. PDGF is also stored in the alpha-granules of platelets and is released upon adherence to traumatised tissues. PDGF is a dimeric glycoprotein formed by two A chains (AA), two B chains (BB), or as a heterodimer with an A and a B chain (AB). The PDGF dimer binds the cell surface receptor tyrosine kinases PDGFR-α and PDGFR-β.
Numéro de catalogue:
(BOSSBS-10133R-HRP)
Fournisseur:
Bioss
Description:
AKT1-specific substrates have been recently identified, including palladin (PALLD), which phosphorylation modulates cytoskeletal organization and cell motility; prohibitin (PHB), playing an important role in cell metabolism and proliferation; and CDKN1A, for which phosphorylation at 'Thr-145' induces its release from CDK2 and cytoplasmic relocalization. These recent findings indicate that the AKT1 isoform has a more specific role in cell motility and proliferation. Phosphorylates CLK2 thereby controlling cell survival to ionizing radiation.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-10133R-FITC)
Fournisseur:
Bioss
Description:
AKT1-specific substrates have been recently identified, including palladin (PALLD), which phosphorylation modulates cytoskeletal organization and cell motility; prohibitin (PHB), playing an important role in cell metabolism and proliferation; and CDKN1A, for which phosphorylation at 'Thr-145' induces its release from CDK2 and cytoplasmic relocalization. These recent findings indicate that the AKT1 isoform has a more specific role in cell motility and proliferation. Phosphorylates CLK2 thereby controlling cell survival to ionizing radiation.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-6637R-A488)
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-5203R-A750)
Fournisseur:
Bioss
Description:
Autophagy is the process by which endogenous proteins and damaged organelles are destroyed intracellularly. Autophagy is postulated to be essential for cell homeostasis and cell remodeling during differentiation, metamorphosis, non-apoptotic cell death, and aging. Reduced levels of autophagy have been described in some malignant tumors, and a role for autophagy in controlling the unregulated cell growth linked to cancer has been proposed. This gene encodes a member of the autophagin protein family. The encoded protein is also designated as a member of the C-54 family of cysteine proteases.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-0876R-A680)
Fournisseur:
Bioss
Description:
AKT1-specific substrates have been recently identified, including palladin (PALLD), which phosphorylation modulates cytoskeletal organization and cell motility; prohibitin (PHB), playing an important role in cell metabolism and proliferation; and CDKN1A, for which phosphorylation at 'Thr-145' induces its release from CDK2 and cytoplasmic relocalisation. These recent findings indicate that the AKT1 isoform has a more specific role in cell motility and proliferation. Phosphorylates CLK2 thereby controlling cell survival to ionizing radiation.
UOM:
1 * 100 µl
Numéro de catalogue:
(BOSSBS-10133R-A488)
Fournisseur:
Bioss
Description:
AKT1-specific substrates have been recently identified, including palladin (PALLD), which phosphorylation modulates cytoskeletal organization and cell motility; prohibitin (PHB), playing an important role in cell metabolism and proliferation; and CDKN1A, for which phosphorylation at 'Thr-145' induces its release from CDK2 and cytoplasmic relocalization. These recent findings indicate that the AKT1 isoform has a more specific role in cell motility and proliferation. Phosphorylates CLK2 thereby controlling cell survival to ionizing radiation.
UOM:
1 * 100 µl
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