Breast most cancers (BC) is without doubt one of the most typical causes of demise amongst ladies worldwide. Just lately, curiosity in novel approaches for BC has elevated by creating new medicine derived from pure merchandise with decreased unwanted effects. This examine aimed to deal with BC cells with harmine hydrochloride (HMH) to establish its anticancer results and mechanisms.
HMH therapy suppressed cell development, migration, invasion, and colony formation in MCF-7 and MDA-MB-231 cells, whatever the hormone signaling. It additionally decreased the phosphorylation of PI3K, AKT, and mTOR and elevated FOXO3a expression. Moreover, HMH therapy elevated p38 phosphorylation in MCF-7 cells and activated c-Jun N-terminal kinase (JNK) phosphorylation in MDA-MB-231 cells in a dose-dependent method, the place activated p38 and JNK elevated FOXO3a expression.
Activated FOXO3a elevated the expression of p53, p21, and their downstream proteins, together with p-cdc25, p-cdc2, and cyclin B1, to induce G2/M cell cycle arrest. Moreover, HMH inhibited the PI3K/AKT/mTOR pathway by considerably decreasing p-AKT expression together with LY294002, an AKT inhibitor. These outcomes point out that mitogen-activated protein kinases (MAPKs) and AKT/FOXO3a signaling pathways mediate the induction of cell cycle arrest following HMH therapy. Subsequently, HMH may very well be a possible energetic compound for anticancer bioactivity in BC cells.
Diosmetin inhibits cell development and proliferation by regulating the cell cycle and lipid metabolism pathway in hepatocellular carcinoma
Diosmetin (DSM), a newly found pure flavonoid, present in citrus crops and olive leaves, has been reported to inhibit the development of most cancers when used as a meals complement. This examine aimed to research DSM’s anti-hepatocellular carcinoma (HCC) properties and potential molecular mechanisms. Hep3B and HCCLM3 cells have been chosen to judge the anti-HCC properties of DSM in vitro. RNA sequencing (RNA-seq) was used to establish the potential molecular targets and pathways.
Gasoline chromatography-mass spectrometry (GC-MS) was used to judge the impact of DSM therapy on the first metabolites of HCCLM3 cells. Tumor xenograft was carried out in nude mice to look at the anti-HCC properties of DSM in vivo. The outcomes confirmed that DSM inhibited the proliferation and migration of HCC cells in vitro in a dose-dependent method.
RNA-seq recognized 4459 differentially expressed genes (DEGs) that have been extremely enriched within the cell cycle pathway. As well as, DSM regulated cell development by arresting the cell cycle within the G1 part by lowering the expression of BCL2, CDK1, and CCND1. Moreover, metabolomics evaluation revealed that DSM interfered with the lipid metabolism pathway of HCC cells by considerably inhibiting the synthesis of metabolites, comparable to acetic acid, decanoic acid, glycerol, and L-proline.
Subcutaneous tumor formation experiments revealed that DSM considerably decreased the tumor quantity and weight when in comparison with the management. Immunohistochemical evaluation additional revealed that DSM therapy considerably decreased the expression of the proliferative marker KI67. Our findings demonstrated that DSM exhibited antitumor results on HCC cells by inhibiting cell proliferation by way of cell cycle arrest and interfering with lipid metabolism.
Myricetin Induces Autophagy and Cell Cycle Arrest of HCC by Inhibiting MARCH1-Regulated Stat3 and p38 MAPK Signaling Pathways
Myricetin is a kind of pure flavonol recognized for its anticancer exercise. Nevertheless, the molecular mechanism of myricetin in anti-hepatocellular carcinoma (HCC) will not be nicely outlined. Earlier research indicated that downregulation of membrane-associated RING-CH finger protein 1 (MARCH1) contributed to the therapy of a wide range of cancers.
Whether or not the anticancer property of myricetin is related to MARCH1 expression stays to be investigated. This analysis explored the anti-HCC mechanism of myricetin. Our outcomes point out that myricetin induces autophagy and arrests cell cycle on the G2/M part to suppress the proliferation of HCC cells by downregulating MARCH1. Myricetin reduces MARCH1 protein in Hep3B and HepG2 cells. Curiously, myricetin upregulates the MARCH1 mRNA stage in Hep3B cells however downregulates it in HepG2 cells.
The knockdown of MARCH1 by siRNAs (small interfering RNAs) decreases the phosphorylated p38 MAPK (p-p38 MAPK) and Stat3 (p-Stat3), and inhibits HCC cell viability. Furthermore, myricetin inhibits p38 MAPK and Stat3 signaling pathways by downregulating MARCH1 to repress HCC development each in vitro and in vivo. Bafilomycin A1 (BafA1), an autophagy inhibitor, has synergetic impact with myricetin to inhibit HCC development.
Taken collectively, our outcomes reveal that myricetin inhibits the proliferation of HCC cells by inhibiting MARCH1-regulated p38 MAPK and Stat3 signaling pathways. This analysis offers a brand new molecular mechanism for myricetin in anti-HCC and means that focusing on MARCH1 may very well be a novel therapy technique in creating anticancer therapeutics.
Delphinidin induces cell cycle arrest and apoptosis in HER-2 optimistic breast most cancers cell traces by regulating the NF-κB and MAPK signaling pathways
Delphinidin is an anthocyanidin monomer, generally present in greens and fruits, and has demonstrated antitumor results within the HER-2-positive MDA-MB-453 breast most cancers cell line, with low cytotoxicity on regular breast cells. Nevertheless, the direct purposeful mechanisms underlying the impact of delphinidin on HER-2-positive breast most cancers cells has not been absolutely characterised.
Within the current examine, it was discovered that delphinidin may induce G2/M part cell cycle arrest by inhibiting the protein expression stage of cyclin B1 and Cdk1 in HER-2-positive breast most cancers cell traces. As well as, delphinidin promoted the mitochondrial apoptosis pathway by inhibiting the ERK and NF-κB signaling pathway and activating the JNK signaling pathway.
Subsequently, delphinidin markedly suppressed the viability of the HER-2-positive breast most cancers cell traces by modulating the cell cycle and inducing apoptosis. Total, the findings from the current examine demonstrated that delphinidin therapy may induce the mitochondrial apoptosis pathway in human HER-2-positive breast most cancers cell traces, offering an experimental foundation for the prevention and therapy of HER-2-positive breast most cancers by flavonoids.
Dioscin Decreases Breast Most cancers Stem-like Cell Proliferation by way of Cell Cycle Arrest by Modulating p38 Mitogen-activated Protein Kinase and AKT/mTOR Signaling Pathways
Dioscin (DS), a steroidal saponin, has been proven to have anti-cancer exercise by exerting antioxidant results and inducing apoptosis. Nevertheless, the anti-cancer exercise of DS in breast cancer-derived stem cells continues to be controversial.
The aim of this examine was to judge the results of DS on migration, invasion, and colony formation in MDA-MB-231 and MCF-7 cell traces and the mechanism by which it inhibits proliferation of breast most cancers stem-like cells after inducing differentiation into breast most cancers stem cells. DS therapy considerably decreased mobile migration, invasion, and colony formation in MDA-MB-231 and MCF-7 cells.
Throughout the differentiation course of that induced manifestation of breast most cancers stem-like cells, DS considerably inhibited mammosphere formation in a dose-dependent method and elevated the expression of p53 and p21 in breast most cancers stem-like cells, decreasing the expression of cdc2 and cyclin B1 in MDA-MB-231 cells and cyclin D, cyclin E, CDK4, and CDK2 in MCF-7 cells.
Gli Reporter - NIH3T3 Cell line (Hedgehog Pathway) |
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GWB-PS8936 | GenWay Biotech | 500reactions | Ask for price |
SRE eGPF Reporter - HEK293 Cell Line (ERK Pathway) |
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78327 | BPS Bioscience | 2 vials | EUR 2275 |
Description: Recombinant HEK-293 cells expressing enhanced green fluorescent protein (eGFP) under the control of SRE responsive elements. This cell line is validated for its response to EGF or serum stimulation and to treatment with inhibitors of ERK signaling pathway. |
NFAT Reporter - Hek293 Cell Line (PKC/ Ca2+ Pathway) |
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79298 | BPS Bioscience | 2 vials | EUR 2140 |
Description: The NFAT Reporter - Hek293 cell line contains a firefly luciferase gene under the control of NFAT response element stably integrated into Hek293 cells. This cell line is validated for the response to the stimulation of phorbol 12-myristate 13-acetate (PMA) with ionomycin. |
Human Hippo Pathway TEAD Reporter Cell Line-MCF7 |
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ABC-RC0094 | AcceGen | 1 vial | Ask for price |
Description: Human Hippo Pathway TEAD Reporter Cell Line is derived from MCF7. It can be used for monitoring Hippo pathway activity and screen for activators or inhibitors of the Hippo pathway. |
Hippo Pathway TEAD Luciferase Reporter MCF7 cell line |
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60618 | BPS Bioscience | 2 vials | EUR 2445 |
Description: The TEAD Reporter - MCF7 cell line contains the firefly luciferase gene under the control of TEAD responsive elements stably integrated into the human breast cancer cell line, MCF7. Inside the cells, basal unphosphorylated YAP/TAZ remains in the nucleus and induces the constitutive expression of luciferase reporter. The cell line is validated for the inhibition of the expression of luciferase reporter by the activators of the Hippo pathway. |
ARE Reporter – HepG2 Cell line (Nrf2 Antioxidant Pathway) |
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60513 | BPS Bioscience | 2 vials | EUR 2445 |
Description: The ARE Reporter - Hep G2 cell line is designed to monitor Nrf2 antioxidant response pathway. The cell contains a firefly luciferase gene under the control of ARE (antioxidant response element) stably integrated into Hep G2 cells. |
Myc Report Cell Line(Luc)–HCT116 (Myc Signaling Pathway) |
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ABC-RC115D | AcceGen | 1 vial | Ask for price |
Description: The Myc Reporter andndash; HCT116 cell line contains the firefly luciferase gene under the control of Myc responsive elements stably integrated into HCT116 cells, a human colon cancer cell line. HCT116 contains a mutated beta-catenin which leads to the accumulation of andbeta; -catenin and constitutive activation of downstream Myc that induces the expression of Myc luciferase reporter. The cell line is validated for the inhibition of the expression of Myc luciferase reporter. |
ISRE Reporter-HEK293 Recombinant Cell Line (JAK pathway) |
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60510 | BPS Bioscience | 2 vials | EUR 2275 |
Description: The ISRE Reporter - HEK293 Cell Line is designed for monitoring the activity of the JAK/STAT signaling pathway. The ISRE Reporter - HEK293 Cell Line contains the firefly luciferase gene under the control of ISRE stably integrated into HEK293 cells. |
AP-1 Reporter - HEK293 Cell Line (JNK signaling pathway) |
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60405 | BPS Bioscience | 2 vials | EUR 2445 |
Description: The AP-1 Reporter - HEK293 Cell Linee is designed for monitoring the activity of the JNK signaling pathway. The AP1 Reporter - HEK293 cell line contains a firefly luciferase gene under the control of AP1-responsive elements that are stably integrated into HEK293 cells. |
AP-1 Report Cell Line-HEK293(JNK signaling pathway) |
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ABC-RC119D | AcceGen | 1 vial | Ask for price |
Description: The AP-1 Reporter – HEK293 Cell Line is designed for monitoring the activity of the JNK signaling pathway. The AP1 Reporter – HEK293 cell line contains a firefly luciferase gene under the control of AP1-responsive elements that are stably integrated into HEK293 cells. |
AP-1 Reporter - HEK293 Cell Line (JNK signaling pathway) |
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GWB-PS7F15 | GenWay Biotech | 1.5x10^6cells | Ask for price |
Myc Reporter (Luc) - HCT116 Cell Line (Myc Signaling Pathway) |
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60520 | BPS Bioscience | 2 vials | EUR 2175 |
Description: The Myc Reporter - HCT116 cell line contains the firefly luciferase gene under the control of Myc responsive elements stably integrated into HCT116 cells, a human colon cancer cell line. HCT116 contains a mutated beta-catenin which leads to the accumulation of β-catenin and constitutive activation of downstream Myc that induces the expression of Myc luciferase reporter. The cell line is validated for the inhibition of the expression of Myc luciferase reporter. |
TGF/SMAD Signaling Pathway SBE Reporter - HEK293 Cell Line |
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60653 | BPS Bioscience | 2 vials | EUR 2505 |
Description: The SBE Reporter - HEK293 Cell Line is designed for monitoring the activity of the TGF /SMAD signaling pathway. The transforming growth factor beta (TGF ) signaling pathway is involved in a diverse range of cell processes such as differentiation, cell cycle arrest, and immune regulation. TGF signaling has been linked to cardiac disease, cancer, Alzheimer's and other human diseases. TGF proteins bind to receptors on the cell surface, initiating a signaling cascade that leads to phosphorylation and activation of SMAD2 and SMAD3, which then form a complex with SMAD4. The SMAD complex then translocates to the nucleus and binds to the SMAD binding element (SBE) in the nucleus, leading to transcription and expression of TGF / SMAD responsive genes. |
TGF/SMAD Signaling Pathway SBE Report Cell Line-HEK293 |
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ABC-RC122D | AcceGen | 1 vial | Ask for price |
Description: The SBE Reporter andndash; HEK293 Cell Line is designed for monitoring the activity of the TGF /SMAD signaling pathway. The transforming growth factor beta (TGF) signaling pathway is involved in a diverse range of cell processes such as differentiation, cell cycle arrest, and immune regulation. TGF signaling has been linked to cardiac disease, cancer, Alzheimerandrsquo;s and other human diseases. TGF proteins bind to receptors on the cell surface, initiating a signaling cascade that leads to phosphorylation and activation of SMAD2 and SMAD3, which then form a complex with SMAD4. The SMAD complex then translocates to the nucleus and binds to the SMAD binding element (SBE) in the nucleus, leading to transcription and expression of TGF / SMAD responsive genes. |
GAS Reporter (Luc) - HeLa Cell Line (IFNγ/JAK/STAT1 Pathway) |
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79041 | BPS Bioscience | 2 vials | EUR 1810 |
Description: The GAS reporter (Luc)-HeLa cell line is designed to monitor the activity of interferon gamma-induced signal transduction pathways in cultured cells by measuring activated STAT1 homodimers. It contains a firefly luciferase gene driven by three copies of the interferon gamma-activated sites (GAS) located upstream of the minimal TATA promoter. IFNγ first binds to a heterodimeric receptor consisting of two chains, IFNGR1 and IFNGR2, causing its dimerization and the activation of specific Janus family kinases (JAK1 and JAK2). Two STAT1 molecules associate with this ligand-activated receptor complex and are activated by phosphorylation to form active homodimer. The active STAT1 homodimers translocate to the nucleus where they bind interferon gamma-activated sites (GAS) in the promoter of IFNγ inducible genes, including luciferase reporter gene. |
Notch Signaling Pathway Notch1/CSL Reporter - HEK293 Cell Line |
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60652 | BPS Bioscience | 2 vials | EUR 2175 |
Description: The Notch CSL Reporter - HEK293 cell line contains the firefly luciferase gene under the control of Notch-response elements (CSL responsive elements) alone with expression construct for Notch1 E (NOTCH1 that has a deletion of the entire extracellular domain) stably integrated into HEK293 cells. Inside the cells, the Notch1 E can be cleaved by γ-secretase. The active Notch1 NICD is released to nucleus and induces the constitutive expression of luciferase reporter. The cell line is validated for the inhibition of the expression of luciferase reporter using a known inhibitor of the Notch signaling pathway. |
Notch Signaling Pathway Notch1/CSL Report Cell Line-HEK293 |
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ABC-RC123D | AcceGen | 1 vial | Ask for price |
Description: The Notch CSL Reporter andndash; HEK293 cell line contains the firefly luciferase gene under the control of Notch-response elements (CSL responsive elements) alone with expression construct for Notch1 E (NOTCH1 that has a deletion of the entire extracellular domain) stably integrated into HEK293 cells. Inside the cells, the Notch1 E can be cleaved by andgamma;-secretase. The active Notch1 NICD is released to nucleus and induces the constitutive expression of luciferase reporter. The cell line is validated for the inhibition of the expression of luciferase reporter using a known inhibitor of the Notch signaling pathway. |
TCF/LEF StemBright™ Luciferase iPS Cell Pool (Wnt Pathway) |
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78515 | BPS Bioscience | 2 vials | EUR 8500 |
Description: The TCF/LEF (T-cell factor/lymphoid enhancing factor) StemBright™ Luciferase Cells contain a firefly luciferase gene under the control of TCF/LEF responsive elements, stably integrated into induced Pluripotent Stem (iPS) cells. TCF/LEF transcription factors are downstream of the Wnt signaling pathway. This cell pool is validated for its response to GSK3β inhibitor CHIR-99021, which activates the Wnt signaling pathway in human pluripotent stem cells. |
Human TGF/SMAD Signaling Pathway SBE Reporter - HEK293 Cell Line |
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ABC-RC0130 | AcceGen | 1 vial | Ask for price |
Description: Human TGF/SMAD Signaling Pathway SBE Reporter Cell Line is derived from HEK293. Application: • Monitor TGF signaling pathway activity.• Screen for activators or inhibitors of the TGF/SMAD signaling pathway. |
Wnt Signaling Pathway TCF/LEF reporter-HEK293 stable cell line |
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GWB-PS34F1 | GenWay Biotech | 1.5x10(6)cells | Ask for price |
CRE/CREB Reporter (Luc) - HEK293 Cell Line (cAMP/PKA Signaling Pathway) |
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60515 | BPS Bioscience | 2 vials | EUR 2070 |
Description: The cAMP/PKA Signaling Pathway CRE/CREB Reporter (Luc) - HEK293 Cell Line is designed for monitoring the activity of the cAMP/ PKA signaling pathway. The cAMP/PKA Signaling Pathway CRE/CREB Reporter (Luc) - HEK293 Cell Line contains a firefly luciferase gene under the control of multimerized cAMP response element (CRE) stably integrated into HEK293 cells. Elevation of the intracellular cAMP level activates cAMP response element binding protein (CREB) to bind CRE and induces the expression of luciferase. |
CRE/CREB Reporter (Luc) - Jurkat Cell Line (cAMP/PKA Signaling Pathway) |
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79636 | BPS Bioscience | 2 vials | EUR 1810 |
Description: The CRE/CREB Reporter (Luc) - Jurkat Cell Line contains a firefly luciferase gene under the control of multimerized cAMP response element (CRE) stably integrated into Jurkat cells. Elevation of the intracellular cAMP level activates cAMP response element binding protein (CREB) to bind CRE and induces the expression of luciferase. This cell line is validated for response to stimulation by Forskolin. |
Human Notch Signaling Pathway Notch1/CSL Reporter Cell Line-HEK293 |
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ABC-RC0116 | AcceGen | 1 vial | Ask for price |
Description: Human Notch Signaling Pathway Notch1/CSL Reporter Cell Line is derived from HEK293. Application: • Monitor Notch signaling pathway activity.• Screen for activators or inhibitors of the Notch signaling pathway. |
GR-GAL4 Reporter (Luc)-HEK293 Cell Line (Glucocorticoid Receptor Pathway) |
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60655 | BPS Bioscience | 2 vials | EUR 2275 |
Description: The Glucocorticoid Receptor Pathway GAL4 Reporter (Luc) - HEK293 Cell Line contains a_x000D_firefly luciferase gene under the control of glucocorticoid receptor ligand binding domain that is_x000D_fused to the DNA binding domain (DBD) of GAL4 (GAL4 DBD-GR) stably integrated into_x000D_HEK293 cells. This fusion construct activates firefly luciferase expression under the control of a_x000D_multimerized GAL4 upstream activation sequence (UAS). This allows for specific detection of_x000D_glucocorticoid-induced activation of the glucocorticoid receptor without the need for individual_x000D_transcriptional targets and with low cross-reactivity for other nuclear receptor pathways. This cell_x000D_line is validated for response to stimulation of dexamethasone and to the treatment with_x000D_mifepristone, an inhibitor of the glucocorticoid signaling pathway. |
TCF/LEF reporter-HEK293 cell line (Wnt Signaling Pathway, Lithium-Dependent) |
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60501 | BPS Bioscience | 2 vials | EUR 2505 |
Description: The Wnt Signaling Pathway TCF/LEF Reporter (Luc) - HEK293 Cell Line is designed for monitoring the activity of the Wnt/b-catenin signaling pathway. The Wnt Signaling Pathway TCF/LEF Reporter (Luc) - HEK293 Cell Line contains a firefly luciferase gene under the control of TCF/LEF responsive elements stably integrated into HEK293 cells. This cell line is validated for the response to the stimulation of mouse Wnt3a and to the treatment with an inhibitor of Wnt/b-catenin signaling pathway. |
IDO Pathway inhibitor |
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2746-250 | Biovision | each | EUR 392.4 |
IDO Pathway inhibitor |
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2746-50 | Biovision | each | EUR 144 |
TCF/LEF Report Cell Line-HEK293(Wnt Signaling Pathway Lithium Chloride Dependent) |
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ABC-RC121D | AcceGen | 1 vial | Ask for price |
Description: The Wnt Signaling Pathway TCF/LEF Reporter (Luc) andndash; HEK293 Cell Line contains a firefly luciferase gene under the control of TCF/LEF responsive elements stably integrated into HEK293 cells. This cell line is validated for the response to the stimulation of mouse and human Wnt3a and to the treatment with an inhibitor of Wnt/andbeta;-catenin signaling pathway. |
Transfection Collection™ : CRE/CREB Transient Pack (cAMP/PKA Cell Signaling Pathway) |
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79267 | BPS Bioscience | 500 rxns. | EUR 715 |
Description: The CRE/CREB Transient Pack is designed to provide the tools necessary for transiently transfecting and monitoring the activity of the cAMP/PKA signaling pathway in cultured cells. The kit contains transfection-ready vectors containing firefly luciferase as a cAMP/PKA pathway-responsive reporter and constitutively expressing Renilla luciferase as a transfection control. It also includes the Dual Luciferase detection reagents to detect both luciferase activities and specialized medium for growing and assaying HEK293 cells._x000D_The key to the CRE/CREB Transient Pack is the CRE/CREB luciferase reporter vector, which is a cAMP/PKA Cell Signaling Pathway-responsive reporter. This reporter contains the firefly luciferase gene under the control of multimerized cAMP response elements (CRE) located upstream of a minimal promoter. Elevation of the intracellular cAMP level activates cAMP response element binding protein (CREB) to bind CRE and induces the expression of luciferase._x000D_The CRE reporter is premixed with constitutively-expressing Renilla (sea pansy) luciferase vector that serves as an internal control for transfection efficiency. The kit also includes a non-inducible firefly luciferase vector premixed with the constitutively-expressing Renilla luciferase vector as a negative control. The non-inducible luciferase vector contains the firefly luciferase gene under the control of a minimal promoter, but without any additional response elements. The negative control is critical to determining pathway-specific effects and background luciferase activity._x000D_Additionally, the pack includes cell culture medium (BPS Medium 1) that has been optimized for use with HEK293 cells*. BPS Medium 1 includes MEM medium, 10% fetal bovine serum, 1% non-essential amino acids, sodium pyruvate, and 1% Pen/Strep. Finally, the pack provides the Dual Luciferase (Firefly-Renilla) Assay System. These luciferase reagents provide highly sensitive, stable detection of firefly luciferase activity and Renilla luciferase activity. The dual luciferase reagents can be used directly in cells in growth medium, and can be detected with any luminometer; automated injectors are not required._x000D_* Other mammalian cell lines may also be used, but an alternate cell culture medium may be required for optimal cell growth. |
Akt Pathway Sampler Kit |
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E051001 | EnoGene | 5x50ug | EUR 475 |
Description: Available in various conjugation types. |
Akt Pathway Sampler Kit |
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MBS8505956-5x005mg | MyBiosource | 5x0.05mg | EUR 575 |
MAPK Pathway Sampler Kit |
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E051017 | EnoGene | 5x50ug | EUR 475 |
Description: Available in various conjugation types. |
NFκB Pathway Sampler Kit |
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E051021 | EnoGene | 5x50ug | EUR 475 |
Description: Available in various conjugation types. |
Wnt pathway inhibitor 3 |
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HY-153750 | MedChemExpress | 10 mg | EUR 54.11 |
Description: Wnt pathway inhibitor 3 is a potent wnt inhibitor with an IC50 value of 45 nM. Wnt pathway inhibitor 3 shows antiproliferative activity[1]. |
Wnt pathway inhibitor 4 |
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HY-153753 | MedChemExpress | 10 mg | EUR 54.11 |
Description: Wnt pathway inhibitor 4 (compound 16D) is an anticancer agent that has anti-proliferative activity[1]. |
Wnt pathway activator 1 |
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MBS133516-INQUIRE | MyBiosource | INQUIRE | Ask for price |
Wnt pathway activator 2 |
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HY-136073 | MedChemExpress | 10 mg | EUR 919.93 |
Description: Wnt pathway activator 2 is a potent Wnt activator extracted from patent WO2012024404A1, compound 2, has an EC50s of 13 nM[1]. |
Wnt pathway activator 1 |
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MBS5755712-10mg | MyBiosource | 10mg | EUR 210 |
Wnt pathway activator 1 |
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MBS5755712-25mg | MyBiosource | 25mg | EUR 305 |
Wnt pathway activator 1 |
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MBS5755712-2mg | MyBiosource | 2mg | EUR 155 |
Wnt pathway activator 1 |
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MBS5755712-50mg | MyBiosource | 50mg | EUR 435 |
Wnt pathway activator 1 |
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MBS5755712-5mg | MyBiosource | 5mg | EUR 180 |
Wnt pathway activator 2 |
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MBS5767862-5mg | MyBiosource | 5mg | EUR 915 |
Wnt pathway activator 2 |
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MBS5767862-5x5mg | MyBiosource | 5x5mg | EUR 3970 |
MAPK Pathway Sampler Kit |
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MBS8504436-5x005mg | MyBiosource | 5x0.05mg | EUR 575 |
Wnt pathway activator 1 |
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T17256-10mg | TargetMol Chemicals | 10mg | Ask for price |
Description: Wnt pathway activator 1 |
Wnt pathway activator 1 |
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T17256-1g | TargetMol Chemicals | 1g | Ask for price |
Description: Wnt pathway activator 1 |
Wnt pathway activator 1 |
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T17256-1mg | TargetMol Chemicals | 1mg | Ask for price |
Description: Wnt pathway activator 1 |
Wnt pathway activator 1 |
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T17256-50mg | TargetMol Chemicals | 50mg | Ask for price |
Description: Wnt pathway activator 1 |
Wnt pathway activator 1 |
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T17256-5mg | TargetMol Chemicals | 5mg | Ask for price |
Description: Wnt pathway activator 1 |
Curiously, DS therapy induced G2/M and G0/G1 cell cycle arrest within the MDA-MB-231 and MCF-7 cells, respectively. DS additionally elevated the phosphorylation of p38 and decreased the expression ranges of p-AKT and p-mTOR. These outcomes counsel that DS regulates the p38 mitogen-activated protein kinase and AKT/mTOR signaling pathways to cut back the proliferation of breast most cancers stem-like cells by cell cycle arrest. Subsequently, these findings counsel that DS could function a possible therapy candidate focusing on breast most cancers stem cells.