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Description: GOLPH3 Antibody: GOLPH3 was initially identified as a peripheral membrane protein localized to the trans-Golgi network, but others reported it to be primarily a mitochondrial protein that regulated the mitochondrial mass through the regulation of the mitochondria-specific phospholipid cardiolipin. GOLPH3 has since been implicated in the target of rapamycin (TOR) signalling pathway. Its overexpression in transfected cells led to and increase in anchorage-independent growth and cell proliferation in vitro. Furthermore, GOLPH3-transfected cells enhanced S6 Kinase activity in response to growth factor stimulation by EGF. Simultaneously, AKT phosphorylation increased in these cells, while these events were abrogated in GOLPH3 siRNA treated cells compared to control cells, indicating the GOLPH3 can enhance signalling through TOR-associated complexes. These results suggest that GOLPH3 is a bona fide oncogene and may be a useful target for therapeutic strategies.
Catalog Number: PRSI5443
UOM: 1 * 100 µG
Supplier: ProSci Inc.


Description: Non-receptor tyrosine-protein kinase implicated in the regulation of a variety of signaling pathways that control the differentiation and maintenance of normal epithelia, as well as tumor growth. Function seems to be context dependent and differ depending on cell type, as well as its intracellular localization. A number of potential nuclear and cytoplasmic substrates have been identified. These include the RNA-binding proteins: KHDRBS1/SAM68, KHDRBS2/SLM1, KHDRBS3/SLM2 and SFPQ/PSF; transcription factors: STAT3 and STAT5A/B and a variety of signaling molecules: ARHGAP35/p19RhoGAP, PXN/paxillin, BTK/ATK, STAP2/BKS. Associates also with a variety of proteins that are likely upstream of PTK6 in various signaling pathways, or for which PTK6 may play an adapter-like role. These proteins include ADAM15, EGFR, ERBB2, ERBB3 and IRS4. In normal or non-tumorigenic tissues, PTK6 promotes cellular differentiation and apoptosis. In tumors PTK6 contributes to cancer progression by sensitizing cells to mitogenic signals and enhancing proliferation, anchorage-independent survival and migration/invasion. Association with EGFR, ERBB2, ERBB3 may contribute to mammary tumor development and growth through enhancement of EGF-induced signaling via BTK/AKT and PI3 kinase. Contributes to migration and proliferation by contributing to EGF-mediated phosphorylation of ARHGAP35/p19RhoGAP, which promotes association with RASA1/p12RasGAP, inactivating RhoA while activating RAS. EGF stimulation resulted in phosphorylation of PNX/Paxillin by PTK6 and activation of RAC1 via CRK/CrKII, thereby promoting migration and invasion. PTK6 activates STAT3 and STAT5B to promote proliferation. Nuclear PTK6 may be important for regulating growth in normal epithelia, while cytoplasmic PTK6 might activate oncogenic signaling pathways. Isoform 2 inhibits PTK6 phosphorylation and PTK6 association with other tyrosine-phosphorylated proteins.
Catalog Number: BOSSBS-12890R-A488
UOM: 1 * 100 µl
Supplier: Bioss


Description: Non-receptor tyrosine-protein kinase implicated in the regulation of a variety of Signalling pathways that control the differentiation and maintenance of normal epithelia, as well as tumour growth. Function seems to be context dependent and differ depending on cell type, as well as its intracellular localisation. A number of potential nuclear and cytoplasmic substrates have been identified. These include the RNA-binding proteins: KHDRBS1/SAM68, KHDRBS2/SLM1, KHDRBS3/SLM2 and SFPQ/PSF; transcription factors: STAT3 and STAT5A/B and a variety of Signalling molecules: ARHGAP35/p19RhoGAP, PXN/paxillin, BTK/ATK, STAP2/BKS. Associates also with a variety of proteins that are likely upstream of PTK6 in various Signalling pathways, or for which PTK6 may play an adapter-like role. These proteins include ADAM15, EGFR, ERBB2, ERBB3 and IRS4. In normal or non-tumourigenic tissues, PTK6 promotes cellular differentiation and apoptosis. In tumours PTK6 contributes to cancer progression by sensitizing cells to mitogenic signals and enhancing proliferation, anchorage-independent survival and migration/invasion. Association with EGFR, ERBB2, ERBB3 may contribute to mammary tumour development and growth through enhancement of EGF-induced Signalling via BTK/AKT and PI3 kinase. Contributes to migration and proliferation by contributing to EGF-mediated phosphorylation of ARHGAP35/p19RhoGAP, which promotes association with RASA1/p12RasGAP, inactivating RhoA while activating RAS. EGF stimulation resulted in phosphorylation of PNX/Paxillin by PTK6 and activation of RAC1 via CRK/CrKII, thereby promoting migration and invasion. PTK6 activates STAT3 and STAT5B to promote proliferation. Nuclear PTK6 may be important for regulating growth in normal epithelia, while cytoplasmic PTK6 might activate oncogenic Signalling pathways. Isoform 2 inhibits PTK6 phosphorylation and PTK6 association with other tyrosine-phosphorylated proteins.
Catalog Number: BOSSBS-12890R-A750
UOM: 1 * 100 µl
Supplier: Bioss


Description: MYCT1 Antibody: MYCT1 was initially identified as a novel target of the c-Myc oncogene in myeloid cells. It is a widely expressed nuclear protein whose overexpression can promote apoptosis, alteration of morphology, enhancement of anchorage-independent cell growth, tumorigenic conversion, promotion of genomic instability, and inhibition of hematopoietic differentiation. MYCT1 binds to the promoters of several c-Myc-regulated genes and it has been suggested that the phenotypes seen in MYCT1-overexpressing cells are a result of the deregulation of these genes. RUNX1-ETO, a fusion protein made up of RUNX1 and ETO, is thought to deregulate the proliferation and responsiveness of human hematopoietic progenitor cells downstream of MYCT1.
Catalog Number: PRSI7031
UOM: 1 * 100 µG
Supplier: ProSci Inc.


Description: Non-receptor tyrosine-protein kinase implicated in the regulation of a variety of signaling pathways that control the differentiation and maintenance of normal epithelia, as well as tumor growth. Function seems to be context dependent and differ depending on cell type, as well as its intracellular localization. A number of potential nuclear and cytoplasmic substrates have been identified. These include the RNA-binding proteins: KHDRBS1/SAM68, KHDRBS2/SLM1, KHDRBS3/SLM2 and SFPQ/PSF; transcription factors: STAT3 and STAT5A/B and a variety of signaling molecules: ARHGAP35/p19RhoGAP, PXN/paxillin, BTK/ATK, STAP2/BKS. Associates also with a variety of proteins that are likely upstream of PTK6 in various signaling pathways, or for which PTK6 may play an adapter-like role. These proteins include ADAM15, EGFR, ERBB2, ERBB3 and IRS4. In normal or non-tumorigenic tissues, PTK6 promotes cellular differentiation and apoptosis. In tumors PTK6 contributes to cancer progression by sensitizing cells to mitogenic signals and enhancing proliferation, anchorage-independent survival and migration/invasion. Association with EGFR, ERBB2, ERBB3 may contribute to mammary tumor development and growth through enhancement of EGF-induced signaling via BTK/AKT and PI3 kinase. Contributes to migration and proliferation by contributing to EGF-mediated phosphorylation of ARHGAP35/p19RhoGAP, which promotes association with RASA1/p12RasGAP, inactivating RhoA while activating RAS. EGF stimulation resulted in phosphorylation of PNX/Paxillin by PTK6 and activation of RAC1 via CRK/CrKII, thereby promoting migration and invasion. PTK6 activates STAT3 and STAT5B to promote proliferation. Nuclear PTK6 may be important for regulating growth in normal epithelia, while cytoplasmic PTK6 might activate oncogenic signaling pathways. Isoform 2 inhibits PTK6 phosphorylation and PTK6 association with other tyrosine-phosphorylated proteins.
Catalog Number: BOSSBS-12890R-FITC
UOM: 1 * 100 µl
Supplier: Bioss


Description: Non-receptor tyrosine-protein kinase implicated in the regulation of a variety of signaling pathways that control the differentiation and maintenance of normal epithelia, as well as tumor growth. Function seems to be context dependent and differ depending on cell type, as well as its intracellular localization. A number of potential nuclear and cytoplasmic substrates have been identified. These include the RNA-binding proteins: KHDRBS1/SAM68, KHDRBS2/SLM1, KHDRBS3/SLM2 and SFPQ/PSF; transcription factors: STAT3 and STAT5A/B and a variety of signaling molecules: ARHGAP35/p19RhoGAP, PXN/paxillin, BTK/ATK, STAP2/BKS. Associates also with a variety of proteins that are likely upstream of PTK6 in various signaling pathways, or for which PTK6 may play an adapter-like role. These proteins include ADAM15, EGFR, ERBB2, ERBB3 and IRS4. In normal or non-tumorigenic tissues, PTK6 promotes cellular differentiation and apoptosis. In tumors PTK6 contributes to cancer progression by sensitizing cells to mitogenic signals and enhancing proliferation, anchorage-independent survival and migration/invasion. Association with EGFR, ERBB2, ERBB3 may contribute to mammary tumor development and growth through enhancement of EGF-induced signaling via BTK/AKT and PI3 kinase. Contributes to migration and proliferation by contributing to EGF-mediated phosphorylation of ARHGAP35/p19RhoGAP, which promotes association with RASA1/p12RasGAP, inactivating RhoA while activating RAS. EGF stimulation resulted in phosphorylation of PNX/Paxillin by PTK6 and activation of RAC1 via CRK/CrKII, thereby promoting migration and invasion. PTK6 activates STAT3 and STAT5B to promote proliferation. Nuclear PTK6 may be important for regulating growth in normal epithelia, while cytoplasmic PTK6 might activate oncogenic signaling pathways. Isoform 2 inhibits PTK6 phosphorylation and PTK6 association with other tyrosine-phosphorylated proteins.
Catalog Number: BOSSBS-12890R-A647
UOM: 1 * 100 µl
Supplier: Bioss


Description: Non-receptor tyrosine-protein kinase implicated in the regulation of a variety of signaling pathways that control the differentiation and maintenance of normal epithelia, as well as tumor growth. Function seems to be context dependent and differ depending on cell type, as well as its intracellular localization. A number of potential nuclear and cytoplasmic substrates have been identified. These include the RNA-binding proteins: KHDRBS1/SAM68, KHDRBS2/SLM1, KHDRBS3/SLM2 and SFPQ/PSF; transcription factors: STAT3 and STAT5A/B and a variety of signaling molecules: ARHGAP35/p19RhoGAP, PXN/paxillin, BTK/ATK, STAP2/BKS. Associates also with a variety of proteins that are likely upstream of PTK6 in various signaling pathways, or for which PTK6 may play an adapter-like role. These proteins include ADAM15, EGFR, ERBB2, ERBB3 and IRS4. In normal or non-tumorigenic tissues, PTK6 promotes cellular differentiation and apoptosis. In tumors PTK6 contributes to cancer progression by sensitizing cells to mitogenic signals and enhancing proliferation, anchorage-independent survival and migration/invasion. Association with EGFR, ERBB2, ERBB3 may contribute to mammary tumor development and growth through enhancement of EGF-induced signaling via BTK/AKT and PI3 kinase. Contributes to migration and proliferation by contributing to EGF-mediated phosphorylation of ARHGAP35/p19RhoGAP, which promotes association with RASA1/p12RasGAP, inactivating RhoA while activating RAS. EGF stimulation resulted in phosphorylation of PNX/Paxillin by PTK6 and activation of RAC1 via CRK/CrKII, thereby promoting migration and invasion. PTK6 activates STAT3 and STAT5B to promote proliferation. Nuclear PTK6 may be important for regulating growth in normal epithelia, while cytoplasmic PTK6 might activate oncogenic signaling pathways. Isoform 2 inhibits PTK6 phosphorylation and PTK6 association with other tyrosine-phosphorylated proteins.
Catalog Number: BOSSBS-12890R-HRP
UOM: 1 * 100 µl
Supplier: Bioss


Description: Non-receptor tyrosine-protein kinase implicated in the regulation of a variety of signaling pathways that control the differentiation and maintenance of normal epithelia, as well as tumor growth. Function seems to be context dependent and differ depending on cell type, as well as its intracellular localization. A number of potential nuclear and cytoplasmic substrates have been identified. These include the RNA-binding proteins: KHDRBS1/SAM68, KHDRBS2/SLM1, KHDRBS3/SLM2 and SFPQ/PSF; transcription factors: STAT3 and STAT5A/B and a variety of signaling molecules: ARHGAP35/p19RhoGAP, PXN/paxillin, BTK/ATK, STAP2/BKS. Associates also with a variety of proteins that are likely upstream of PTK6 in various signaling pathways, or for which PTK6 may play an adapter-like role. These proteins include ADAM15, EGFR, ERBB2, ERBB3 and IRS4. In normal or non-tumorigenic tissues, PTK6 promotes cellular differentiation and apoptosis. In tumors PTK6 contributes to cancer progression by sensitizing cells to mitogenic signals and enhancing proliferation, anchorage-independent survival and migration/invasion. Association with EGFR, ERBB2, ERBB3 may contribute to mammary tumor development and growth through enhancement of EGF-induced signaling via BTK/AKT and PI3 kinase. Contributes to migration and proliferation by contributing to EGF-mediated phosphorylation of ARHGAP35/p19RhoGAP, which promotes association with RASA1/p12RasGAP, inactivating RhoA while activating RAS. EGF stimulation resulted in phosphorylation of PNX/Paxillin by PTK6 and activation of RAC1 via CRK/CrKII, thereby promoting migration and invasion. PTK6 activates STAT3 and STAT5B to promote proliferation. Nuclear PTK6 may be important for regulating growth in normal epithelia, while cytoplasmic PTK6 might activate oncogenic signaling pathways. Isoform 2 inhibits PTK6 phosphorylation and PTK6 association with other tyrosine-phosphorylated proteins.
Catalog Number: BOSSBS-12890R-A350
UOM: 1 * 100 µl
Supplier: Bioss


Description: PAK4 Antibody: The p21-activated kinases (PAKs) are serine-threonine kinases that bind to the active forms of Cdc42 and Rac. They are divided into two groups, the first of which include PAK1, 2 and 3, and can be activated by Cdc42/Rac binding. Group 1 PAKs contain an autoinhibitory domain whose activity is regulated by Cdc42/Rac binding. The group 1 PAKs are known to be involved in cellular processes such as gene transcription, apoptosis, and cell morphology and motility. Much less is known about the second group, which includes PAK4, 5 and 6. These proteins are not activated by Cdc42/Rac binding. PAK4 was initially identified as a novel effector of Cdc42Hs. Co-expression of PAK4 and Cdc42Hs resulted in induction of filopodia and actin polymerization, showing that it is involved in cytoskeletal reorganization. Other experiments have shown PAK4 to be essential for embryonic viability and proper neuronal development. PAK4 has also been implicated in anchorage-independent growth of tumor cells and is required for activation of several cancer prosurvival pathways.
Catalog Number: PRSI3077
UOM: 1 * 100 µG
Supplier: ProSci Inc.


Description: TGF-beta-1 is a multifunctional cytokine that belongs to a superfamily of structurally related regulatory proteins, which includes three mammalian TGF-beta isoforms (TGF-beta-1, -beta-2, and -beta-3), activin/inhibins and bone morphogenetic proteins. The most abundant isoform, TGF-beta-1, is a 25 kDa homodimer composed of two 12.5 kDa subunits joined by disulfide bonds. TGF-beta-1 is a highly conserved molecule - the amino acid sequence between human and mouse differ only by one residue. Although originally defined by its ability to cause anchorage independent cell growth and changes in cell morphology of rat fibroblasts, subsequent research has revealed that TGF-beta is actually a major growth inhibitor for most cell types. It is produced by a wide variety of cell and tissue types during all stages of cell differentiation. TGF-beta-1 sources include platelets, bone and soft tissues such as placenta and kidneys.
Catalog Number: PRSI49-553
UOM: 1 * 50 µG
Supplier: ProSci Inc.


Description: CELLine™ is a disposable, two-compartment bioreactor manufactured from optically clear virgin PS with a gas transfer bottom made of a moulded silicone membrane providing a 0,2 µm vent barrier. The compartments are separated by a 10 kDa semi-permeable cellulose acetate membrane and individually pressure tested for integrity. CELLine™ classic (CL) is ideal for laboratory scale applications using suspension cells or adherent cells in combination with microcarriers. The unit is optimised for cultivation of hybridomas and many other cell types (for example CHO, NSO, SF cells). CELLine™ adhere (AD) is specifically adapted to allow growth of anchorage-dependent cells (for example HEK, BHK, CHO cells). The CELLine™ AD bioreactor contains a woven PET matrix in the cell compartment providing an ideal surface for cell attachment.
Catalog Number: 392-1007
UOM: 1 * 1 items
Supplier: DWK Life Sciences


Description: The E-Cube™ System is a simple bioreactor with 8500 cm² cell growth area for growing anchorage dependent cells in only a 25,4×35,6 cm footprint. The E-Cube™ System provides a simple method to determine if cells will grow in the CellCube® Module prior to investing in the resources and funding that would be necessary for the larger, automated CellCube® System. Peristaltic pump, CO₂ incubator and medium are not provided.
Catalog Number: 734-4053
UOM: 1 * 1 KIT
Supplier: Corning

Environmentally Preferable


Description: In-line filter, Avantor® Hichrom, Pk: 5
Catalog Number: HICHHI-674
UOM: 1 * 5 items
Supplier: Avantor


Description: This is a fingertight bioanalytical inline filter, comprising a PEEK holder and a 5 μm titanium PEEK-encased frit.
Catalog Number: HICHHI-683
UOM: 1 * 1 items
Supplier: Avantor


Description: In-line filter, Avantor® Hichrom, Pk: 10
Catalog Number: HICHHI-611
UOM: 1 * 10 items
Supplier: Avantor


Description: Lid seal for VAPOUR-Line 135 model, For: VAPOUR-Line 135/135M
Catalog Number: 481-0705
UOM: 1 * 1 items
Supplier: VWR Collection


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