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1,4-Diazabicyclo[2.2.2]octanebis(sulphur+dioxide)adduct
Artikel-Nr:
(BOSSBS-3504R-A488)
Lieferant:
Bioss
Hersteller-Artikelnummer::
BS-3504R-A488
Lokale Artikelnummer::
BOSSBS-3504R-A488
Beschreibung:
Stress-activated, pro-apoptotic kinase which, following caspase-cleavage, enters the nucleus and induces chromatin condensation followed by internucleosomal DNA fragmentation. Key component of the Hippo signaling pathway which plays a pivotal role in organ size control and tumor suppression by restricting proliferation and promoting apoptosis. The core of this pathway is composed of a kinase cascade wherein STK3/MST2 and STK4/MST1, in complex with its regulatory protein SAV1, phosphorylates and activates LATS1/2 in complex with its regulatory protein MOB1, which in turn phosphorylates and inactivates YAP1 oncoprotein and WWTR1/TAZ. Phosphorylation of YAP1 by LATS2 inhibits its translocation into the nucleus to regulate cellular genes important for cell proliferation, cell death, and cell migration. STK3/MST2 and STK4/MST1 are required to repress proliferation of mature hepatocytes, to prevent activation of facultative adult liver stem cells (oval cells), and to inhibit tumor formation (By similarity). Phosphorylates 'Ser-14' of histone H2B (H2BS14ph) during apoptosis. Phosphorylates FOXO3 upon oxidative stress, which results in its nuclear translocation and cell death initiation. Phosphorylates MOBKL1A, MOBKL1B and RASSF2. Phosphorylates TNNI3 (cardiac Tn-I) and alters its binding affinity to TNNC1 (cardiac Tn-C) and TNNT2 (cardiac Tn-T). Phosphorylates FOXO1 on 'Ser-212' and regulates its activation and stimulates transcription of PMAIP1 in a FOXO1-dependent manner. Phosphorylates SIRT1 and inhibits SIRT1-mediated p53/TP53 deacetylation, thereby promoting p53/TP53 dependent transcription and apoptosis upon DNA damage. Acts as an inhibitor of PKB/AKT1. Phosphorylates AR on 'Ser-650' and suppresses its activity by intersecting with PKB/AKT1 signaling and antagonizing formation of AR-chromatin complexes.
VE:
1 * 100 µl
Artikel-Nr:
(BOSSBS-3504R-A680)
Lieferant:
Bioss
Hersteller-Artikelnummer::
BS-3504R-A680
Lokale Artikelnummer::
BOSSBS-3504R-A680
Beschreibung:
Stress-activated, pro-apoptotic kinase which, following caspase-cleavage, enters the nucleus and induces chromatin condensation followed by internucleosomal DNA fragmentation. Key component of the Hippo signaling pathway which plays a pivotal role in organ size control and tumor suppression by restricting proliferation and promoting apoptosis. The core of this pathway is composed of a kinase cascade wherein STK3/MST2 and STK4/MST1, in complex with its regulatory protein SAV1, phosphorylates and activates LATS1/2 in complex with its regulatory protein MOB1, which in turn phosphorylates and inactivates YAP1 oncoprotein and WWTR1/TAZ. Phosphorylation of YAP1 by LATS2 inhibits its translocation into the nucleus to regulate cellular genes important for cell proliferation, cell death, and cell migration. STK3/MST2 and STK4/MST1 are required to repress proliferation of mature hepatocytes, to prevent activation of facultative adult liver stem cells (oval cells), and to inhibit tumor formation (By similarity). Phosphorylates 'Ser-14' of histone H2B (H2BS14ph) during apoptosis. Phosphorylates FOXO3 upon oxidative stress, which results in its nuclear translocation and cell death initiation. Phosphorylates MOBKL1A, MOBKL1B and RASSF2. Phosphorylates TNNI3 (cardiac Tn-I) and alters its binding affinity to TNNC1 (cardiac Tn-C) and TNNT2 (cardiac Tn-T). Phosphorylates FOXO1 on 'Ser-212' and regulates its activation and stimulates transcription of PMAIP1 in a FOXO1-dependent manner. Phosphorylates SIRT1 and inhibits SIRT1-mediated p53/TP53 deacetylation, thereby promoting p53/TP53 dependent transcription and apoptosis upon DNA damage. Acts as an inhibitor of PKB/AKT1. Phosphorylates AR on 'Ser-650' and suppresses its activity by intersecting with PKB/AKT1 signaling and antagonizing formation of AR-chromatin complexes.
VE:
1 * 100 µl
Artikel-Nr:
(BOSSBS-2908R-A750)
Lieferant:
Bioss
Hersteller-Artikelnummer::
BS-2908R-A750
Lokale Artikelnummer::
BOSSBS-2908R-A750
Beschreibung:
Stress-activated serine/threonine-protein kinase involved in cytokines production, endocytosis, reorganisation of the cytoskeleton, cell migration, cell cycle control, chromatin remodeling, DNA damage response and transcriptional regulation. Following stress, it is phosphorylated and activated by MAP kinase p38-alpha/MAPK14, leading to phosphorylation of substrates. Phosphorylates serine in the peptide sequence, Hyd-X-R-X(2)-S, where Hyd is a large hydrophobic residue. Phosphorylates ALOX5, CDC25B, CDC25C, ELAVL1, HNRNPA, HSF1, HSP27/HSPB1, KRT18, KRT2, LIMK1, LSP1, PABPC1, PARN, PDE4A, RCSD1, RPS6KA3, TAB3 and TTP/ZFP36. Mediates phosphorylation of HSP27/HSPB1 in response to stress, leading to dissociate HSP27/HSPB1 from large small heat-shock protein (sHsps) oligomers and impair their chaperone activities and ability to protect against oxidative stress effectively. Involved in inflammatory response by regulating tumor necrosis factor (TNF) and IL6 production post-transcriptionally: acts by phosphorylating AU-rich elements (AREs)-binding proteins ELAVL1, HNRNPA, PABPC1 and TTP/ZFP36, leading to regulate the stability and translation of TNF and IL6 mRNAs. Phosphorylation of TTP/ZFP36, a major post-transcriptional regulator of TNF, promotes its binding to 14-3-3 proteins and reduces its ARE mRNA affinity leading to inhibition of dependent degradation of ARE-containing transcript. Also involved in late G2/M checkpoint following DNA damage through a process of post-transcriptional mRNA stabilisation: following DNA damage, relocalises from nucleus to cytoplasm and phosphorylates HNRNPA and PARN, leading to stabilise GADD45A mRNA. Involved in toll-like receptor signaling pathway (TLR) in dendritic cells: required for acute TLR-induced macropinocytosis by phosphorylating and activating RPS6KA3.
VE:
1 * 100 µl
Lieferant:
PanReac AppliChem
Beschreibung:
Dimethylsulfoxid ≥99,5%, BioChemica® Reagenz für die Zellkultur
Artikel-Nr:
(MSPPEK710742)
Lieferant:
MARKET SOURCE PART PROCESS
Beschreibung:
Human 14-3-3 protein (14-3-3) elisa kit 1 * 96 Tests
VE:
1 * 96 Tests
New Product
Artikel-Nr:
(MSPPC-14)
Lieferant:
MARKET SOURCE PART PROCESS
Hersteller-Artikelnummer::
C-14
Lokale Artikelnummer::
MSPPC-14
Beschreibung:
Cover for WB-14/WBS-14/WBS-14D 1 * 1 ST
VE:
1 * 1 ST
 This is a MarketSource item. Additional charges may apply
Artikel-Nr:
(BOSSBS-4985R-CY3)
Lieferant:
Bioss
Hersteller-Artikelnummer::
BS-4985R-CY3
Lokale Artikelnummer::
BOSSBS-4985R-CY3
Beschreibung:
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.
VE:
1 * 100 µl
Artikel-Nr:
(BOSSBS-4985R)
Lieferant:
Bioss
Hersteller-Artikelnummer::
BS-4985R
Lokale Artikelnummer::
BOSSBS-4985R
Beschreibung:
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.
VE:
1 * 100 µl
Artikel-Nr:
(MSPP2107-7-01-100G)
Lieferant:
MARKET SOURCE PART PROCESS
Hersteller-Artikelnummer::
2107-7-01-100G
Lokale Artikelnummer::
MSPP2107-7-01-100G
Beschreibung:
1-Chloro-2,2,2-trifluoroethyl difluoromethyl ether,99% 1 * 100 g
VE:
1 * 100 g
This is a MarketSource item. Additional charges may apply
Lieferant:
Thermo Scientific
Beschreibung:
Dimethylsulfoxid 99.8+%, reinst
Artikel-Nr:
(KRAF22761.1700)
Lieferant:
Bernd Kraft
Hersteller-Artikelnummer::
22761.1700
Lokale Artikelnummer::
KRAF22761.1700
Beschreibung:
Reag. Ph. Eur.. Kapitel 2.2.2 1 * 250 mL
VE:
1 * 250 mL
Lieferant:
FLUOROCHEM
Beschreibung:
3'-Chlor-2,2,2,4'-tetrafluoracetophenon
Artikel-Nr:
(BOSSBS-3237R-A680)
Lieferant:
Bioss
Hersteller-Artikelnummer::
BS-3237R-A680
Lokale Artikelnummer::
BOSSBS-3237R-A680
Beschreibung:
Serine kinase that plays an essential role in the NF-kappa-B signaling pathway which is activated by multiple stimuli such as inflammatory cytokines, bacterial or viral products, DNA damages or other cellular stresses. Acts as part of the canonical IKK complex in the conventional pathway of NF-kappa-B activation and phosphorylates inhibitors of NF-kappa-B on serine residues. These modifications allow polyubiquitination of the inhibitors and subsequent degradation by the proteasome. In turn, free NF-kappa-B is translocated into the nucleus and activates the transcription of hundreds of genes involved in immune response, growth control, or protection against apoptosis. Negatively regulates the pathway by phosphorylating the scaffold protein TAXBP1 and thus promoting the assembly of the A20/TNFAIP3 ubiquitin-editing complex (composed of A20/TNFAIP3, TAX1BP1, and the E3 ligases ITCH and RNF11). Therefore, CHUK plays a key role in the negative feedback of NF-kappa-B canonical signaling to limit inflammatory gene activation. As part of the non-canonical pathway of NF-kappa-B activation, the MAP3K14-activated CHUK/IKKA homodimer phosphorylates NFKB2/p100 associated with RelB, inducing its proteolytic processing to NFKB2/p52 and the formation of NF-kappa-B RelB-p52 complexes. In turn, these complexes regulate genes encoding molecules involved in B-cell survival and lymphoid organogenesis. Participates also in the negative feedback of the non-canonical NF-kappa-B signaling pathway by phosphorylating and destabilising MAP3K14/NIK. Within the nucleus, phosphorylates CREBBP and consequently increases both its transcriptional and histone acetyltransferase activities. Modulates chromatin accessibility at NF-kappa-B-responsive promoters by phosphorylating histones H3 at 'Ser-10' that are subsequently acetylated at 'Lys-14' by CREBBP. Additionally, phosphorylates the CREBBP-interacting protein NCOA3.
VE:
1 * 100 µl
Artikel-Nr:
(SIALSAB5600139-100)
Lieferant:
Sigma-Aldrich
Hersteller-Artikelnummer::
SAB5600139-100
Lokale Artikelnummer::
SIALSAB5600139-100
Beschreibung:
ANTI-CK-14 (CYTOKERATIN-14) ANTIBODY, RA 1 * 100 l
VE:
1 * 100 µl
Artikel-Nr:
(1.09994.0001)
Lieferant:
Merck
Hersteller-Artikelnummer::
1.09994.0001
Lokale Artikelnummer::
MERC1.09994.0001
Beschreibung:
Vanadium Standard, 1000 mg, Titrisol®, Supelco®, Vanadium, Matrix: 8,6% H₂SO₄, Anwendung: AAS-Standards
VE:
1 * 1 Ampull
Lieferant:
Sigma-Aldrich
Beschreibung:
Silbertrifluoracetat, Sigma-Aldrich®
Preis auf Anfrage
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 noch angezeigt wird und Sie Hilfe benötigen, rufen Sie uns an 1-800-932 - 5000.
Lager für diesen Artikel ist begrenzt, kann aber in einem Lagerhaus in Ihrer Nähe zur Verfügung. Bitte stellen Sie sicher, dass Sie in sind angemeldet auf dieser Seite, so dass verfügbare Bestand angezeigt werden können. Wenn das
noch angezeigt wird und Sie Hilfe benötigen, rufen Sie uns an 1-800-932 - 5000.
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