Activity:. STAT5-IN-1 is a STAT5 inhibitor with an IC50 of 47 μM for STAT5β isoform. IC50 & Target: IC50: 47 μM (STAT5β)[1] In Vitro: The signal transducer and activator of transcription 5 (STAT5) is a member of the STAT family of proteins, implicated in cell growth and differentiation. STAT5-IN-1 inhibits STAT5 by binding to the SH2 domain. The functions of the SH2 domains of STAT3, STAT1, and of the tyrosine kinase Lck are inhibited to a lesser extent (IC50>500 µM). STAT5-IN-1 block STAT5/STAT5 DNA binding in K562 nuclear extracts. Substitution of the hydrogen at C6 of the chromone ring by an ethyl group does not affect activity of STAT5-IN-1 against STAT5β, but leads to complete loss of selectivity against other STAT family members[1]. Protocol:. References:. ...
Among recently investigated potential targets for selective cancer treatment are signal transducers and activators of transcription (STATs). STATs are transcription factors activated in response to cytokines and growth factors and are involved in different cellular processes including proliferation, differentiation and inflammation. Of the seven known mammalian STAT proteins STAT3 was shown to be constitutively activated in many human malignancies. Aberrant STAT3 activity promotes tumor progression through transcriptional activation of genes encoding apoptosis inhibitors, cell-cycle regulators and inducers of angiogenesis. Available data indicate that inhibition of STAT3 signaling leads to an attenuation of cancer cell growth and the induction of apoptosis.. The aim of our investigation was to design a novel STAT3 small molecule inhibitor that would selectively inhibit STAT3 activity, reducing expression of its downstream genes. Thus, we performed computational modeling and small molecule ...
Although the cytokine-inducible transcription factors STAT5a/b promote proliferation of a wide range of cell types, there are cell- and context specific cases in which loss of STAT5a/b results in enhanced cell proliferation. Here we report that loss of STAT5a/b from mouse embryonic fibroblasts (MEFs) leads to enhanced proliferation, which was linked to reduced levels of the cell cycle inhibitor p15INK4B and p21CIP1. We further demonstrate that growth hormone through the transcription factor STAT5a/b enhances expression of the cdkn2B gene and that STAT5a binds to GAS sites within the promoter. We have recently demonstrated that ablation of STAT5a/b from liver results in hepatocellular carcinoma upon a CCl4 insult. We also established that in liver tissue, like in MEFs, STAT5a/b activates expression of the cdkn2B gene. Loss of STAT5a/b led to diminished p15INK4B and increased hepatocyte proliferation. This study for the first time demonstrates that cytokines through STAT5a/b can induce the expression of a
STAT1 makes an essential contribution to innate immunity against viral and intramacrophagic bacterial disease. The objective of our study was to reveal any contribution of non‐tyrosine‐phosphorylated STAT1 to innate immunity. Examining cells and organs of mice expressing a Stat1Y701F mutant, the first observation of note was the strong dependence of STAT1 expression on its tyrosine phosphorylation through tonic signaling. None of the tested stimuli, including L. monocytogenes infection, caused upregulation of the Stat1 gene in the absence of its tyrosine‐phosphorylated product. Therefore, effects of the U‐Stat pathway as defined by Stark and colleagues which rely on an increase in STAT abundance could not be examined. In addition, any results obtained for the immune response of Stat1Y701F cells or mice could not be compared to WT counterparts because a distinction between effects of tyrosine phosphorylation and effects of STAT1 abundance was not possible. To overcome this problem, we ...
Signal transducer and activator of transcription 5 (Stat5) belongs to a family of cytoplasmic transcription factors that can be activated (phosphorylated) by a cell surface receptor. Phosphorylation at Tyr694 is obligatory for Stat5 activation. Stat5 has two isoforms, Stat5 alpha and Stat5 beta. Aberrant Stat5 activation has been implicated in the pathogenesis of chronic myelogenous leukemia, prostate and breast cancer and tumor metastasis. Stat5 is localized in the cytoplasm and upon phosphorylation at Y694 is translocated to the nucleus. Ideal for Cancer, Chromatin & Nuclear Signaling and Signal Transduction research.
The transcription factor STAT6 plays a key role in mediating signaling downstream of the receptors for IL-4 and IL-13. In B cells, STAT6 is required for class switch recombination to IgE and for germinal center formation during type 2 immune responses directed against allergens or helminths. In this study, we compared the transcriptomes and proteomes of primary mouse B cells from wild-type and STAT6-deficient mice cultured for 4 d in the presence or absence of IL-4. Microarray analysis revealed that 214 mRNAs were upregulated and 149 were downregulated ,3-fold by IL-4 in a STAT6-dependent manner. Across all samples, ∼5000 proteins were identified by label-free quantitative liquid chromatography/mass spectrometry. A total of 149 proteins was found to be differentially expressed ,3-fold between IL-4-stimulated wild-type and STAT6−/− B cells (75 upregulated and 74 downregulated). Comparative analysis of the proteome and transcriptome revealed that expression of these proteins was mainly ...
Abstract: : Purpose: STAT proteins are a family of transcription factors that mediate the action of several growth factors. The purpose of this study was to assess the effect of PDGF in STAT1 and STAT3 synthesis. Methods: Primary hRPE cell cultures were established from four human eyes obtained from the Michigan Eye Bank. Cells were allowed to grow to confluence and treated with PDGF and genistein. Cell viability was determined by the trypan blue exclusion method. Cell proliferation was monitored by 3H-thymidine (3H-thy) incorporation. 14C-methionine labeled-intracellular STAT1 and STAT3 synthesis was determined by immunoprecipitation using STAT1 and STAT3 antibodies and SDS-PAGE analysis. Data were analyzed by Student t test and Wilcoxon Signed Rank test. P,0.05 was considered to be significantly different. Results: PDGF increased hRPE cell number and 3H-thymidine incorporation in a dose dependent manner. PDGF also increased 14C-methionine STAT 1 and STAT 3 protein synthesis in a dose ...
The JAK (Janus kinase)/STAT (signal transducer and activator of transcription) signaling pathway transduces stress-activating extracellular chemical signals into cellular responses such as immunity, inflammation, and apoptosis. Cell surface receptors activate JAK proteins, which autophosphorylate, and then phosphorylate the receptor. The STATs are also phosphorylated and activated by the JAKs. Activated STATs homo- or heterodimerize into functional transcription factors, and translocate to the nucleus to initiate target gene transcription. The 4 mammalian JAKs (JAK1, JAK2, JAK3, and TYK2) each recognize different receptors and different STAT proteins. The homo- and heterodimers of the 7 mammalian STATs each have different target genes. JAK/STAT signaling dysregulation commonly occurs in diseases such as atherosclerosis, immunodeficiencies, and cancer ...
Background: The transcription factor Signal Transducer and Activator of Transcription Factor 3 (STAT3) is implicated in acquired drug resistance, metastases and immune suppression in prostate cancer and is a potential target in drug-resistant prostate cancer. Today, the treatment options for metastatic drug-resistant prostate cancer are very limited and existing immunotherapies have so far shown low efficacy. Cancer cells may avoid immune responses by expressing immunosuppressive markers or activating immunosuppressive cells. Myeloid-derived suppressor cells (MDSC) play a major role in the suppression of antitumor immunity and active STAT3 signaling has been shown to be involved in the immunosuppressive functions of these cells. Elevated levels of MDSC have been found in the peripheral blood and at the tumor site of prostate cancer patients and to correlate with disease progression.. Aims: In this study we aimed to investigate if human monocytes could be induced to differentiate into ...
article{2983518, abstract = {Tyrosine phosphorylation is a hallmark for activation of STAT proteins, but their transcriptional activity also depends on other secondary modifications. Type I IFNs can activate both the ISGF3 (STAT1:STAT2:IRF9) complex and STAT3, but with cell-specific, selective triggering of only the ISGF3 transcriptional program. Following a genome-wide RNAi screen, we identified the SIN3 transcription regulator homolog A (Sin3a) as an important mediator of this STAT3-targeted transcriptional repression. Sin3a directly interacts with STAT3 and promotes its deacetylation. SIN3A silencing results in a prolonged nuclear retention of activated STAT3 and enhances its recruitment to the SOCS3 promoter, concomitant with histone hyperacetylation and enhanced STAT3-dependent transcription. Conversely, Sin3a is required for ISGF3-dependent gene transcription and for an efficient IFN-mediated antiviral protection against influenza A and hepatitis C viruses. The Sin3a complex therefore acts ...
It is known that differentiation of Th17 cells is promoted by activation of STAT3 and inhibited by activation of STAT1. Although both transcription factors are activated by several cytokines, including IL-6, IL-21, and IL-27, each of these cytokines has a very different effect on Th17 differentiation, ranging from strong induction (IL-6) to strong inhibition (IL-27). To determine the molecular basis for these differences, we measured STAT3 and STAT1 activation profiles for IL-6, IL-21, and IL-27, as well as for cytokine pairs over time. We found that the ratio of activated STAT3/activated STAT1 is crucial in determining whether cytokines promote or inhibit Th17 differentiation. IL-6 and IL-21 induced p-STAT3/p-STAT1 ratios , 1, leading to the promotion of Th17 differentiation, whereas IL-27 or IL-6+IL-27 induced p-STAT3/p-STAT1 ratios , 1, resulting in inhibition of Th17 differentiation. Consistent with these findings, we show that IL-27 induces sufficient p-STAT3 to promote Th17 differentiation ...
Visconti R., Gadina M., Chiariello M., Chen E.H., Stancato L.F., Gutkind J.S., OShea J.J.. Interleukin-12 (IL-12) is a key immunoregulatory cytokine that promotes Th1 differentiation and cell-mediated immune responses. The transcription factor STAT4 (signal transducer and activator of transcription 4) is an important element in mediating IL-12 signals, as evidenced by the fact that STAT4(-/-) mice display impaired responsiveness to IL-12 and deficient Th1 differentiation. STAT4 is inducibly phosphorylated on tyrosine and serine in response to IL-12, but the kinase(s) responsible for the latter event is unknown. Here we show that IL-12 induces STAT4 phosphorylation on serine 721 and that mutation of serine 721 interferes with STAT4 transcriptional activity. In addition, we show that mutation of tyrosine 693 abrogates IL-12-induced STAT4 tyrosine phosphorylation and transcriptional activity. Although the site surrounding serine 721 is an optimum consensus sequence for mitogen-activated family of ...
Signal transducer and activator of transcription 3 (STAT3) is an important transcription factor ubiquitously expressed in different cell types. STAT3 plays an essential role in cell survival, proliferation, and differentiation. Aberrantly hyper-activated STAT3 signaling in cancer cells and in the tumor microenvironment has been detected in a wide variety of human cancers and is considered an important factor for cancer initiation, development, and progression. However, the role of STAT3 activation in monocytes in the development of HCC has not been well understood. Immunohistochemical analysis of phosphorylated STAT3 was performed on tissue microarray from HCC patients. Using a co-culture system in vivo, HCC cell growth was determined by the MTT assay. In vivo experiments were conducted with mice given diethylinitrosamine (DEN), which induces HCC was used to investigate the role of STAT3 expression in monocytes on tumor growth. Real-time PCR was used to determine the expression of cell proliferation and
Diverse cytokines necessary for normal lymphopoiesis and lymphocyte homeostasis activate STAT5 in responder cells. Although STAT5 has been suggested to be a central molecular effecter of IL-7 function, its essential role during IL-7-dependent T cell development in vivo remained unclear. Using Stat5(-/-) mice we now show that STAT5 is essential for various functions ascribed to IL-7 in vivo. STAT5 is required for embryonic thymocyte production, TCRgamma gene transcription, and Peyers patch development. In sharp contrast, normal STAT5 is dispensable for adult thymopoiesis. In peripheral lymphocytes, STAT5 is primarily required for the generation and/or maintenance of gammadelta T cells and TCRgammadelta(+) intraepithelial lymphocytes. Collectively, these results demonstrate that STAT5 is critical for many, but not all, aspects of steady state lymphoid lineage development and maintenance and suggest the existence of previously undocumented cytokine signaling traits and/or cytokine milieu during adult
An article published in the October 25, 2011 edition of PNAS explored the study of Dr. Francesa Zammarchi et al on the alternative splicing that leads to two isoforms of STAT3: STAT3α and STAT3β. Exon 23, which includes the two amino acid residues necessary for activation of the STAT3 TF, can be fully or partially included in the final product. If the entire exon is included, STAT3α is formed and the protein is fully functional. If the 55 amino acids at the end of exon 23 are excluded from the final product, then STAT3β is made. The premature termination of the protein causes serine 727, a necessary residue for phosphorylation and activation of the STAT3 protein, to be truncated. This renders STAT3β able to maintain its DNA binding function, but not able to be fully active as a transcription factor ...
One subunit of the interleukin-6 (IL-6) receptor, which activates Janus kinases upon ligand binding, is gp130. Tyrosine phosphorylation of gp130 recruits protein phosphatase 2 (SHP2) and signal transducer and activator 3 (STAT3). Ohtani et al. utilized knock-in technology to create mice deficient in only the gp130-mediated SHP2 pathway or the gp130-mediated STAT3 pathway to dissect the roles these two pathways play in IL-6 signaling. Eliminating the SHP2 response resulted in prolonged IL-6-induced STAT3 phosphorylation. STAT3 signaling was required for embryonic development, where as SHP2 signaling-deficient mice were viable and fertile. STAT3 signaling was required for induction of astrocytes by IL-6 cytokines. Reciprocal roles for STAT3 signaling and SHP2 signaling (STAT3 providing a positive signal and SHP2 providing a negative signal) were found for cytokine and immunoglobulin responses and lymphoid organ homeostasis. Thus, mice deficient in SHP2 signaling developed splenomegaly and ...
The Janus kinase (JAK)/STAT signaling pathway is an active focus of MM research. In mononuclear cells from the BM of patients with MM, constitutively activated STAT3 signaling contributes to disease pathogenesis by preventing apoptosis [14]. MM cells express constitutively active forms of nuclear factor-κB and STAT3, and the suppression of these transcription factors inhibits the survival of these malignant cells [15]. Apoptosis has been shown to be induced in diverse MM cells treated with agents that inhibit the STAT3 signaling pathway [1617]. However, few studies have examined the clinical characteristics and prognosis of patients with BM tissue expression of PY-STAT3. Brown et al. [18] used phospho-flow cytometry to evaluate the constitutive expression of phosphorylated STAT3 (pSTAT3), pSTAT5, pERK, pAKT, and IL-6 receptor epitope in cryopreserved BM samples with respect to the clinical significance of positivity. In contrast to our results, the authors found no significant difference in OS ...
This study showed that gp130, a member of the cytokine receptor superfamily, efficiently activates the TAK1 through the YXXQ motif in gp130, and this kinase preferentially activates the downstream kinase NLK, which is responsible for STAT3 Ser-727 phosphorylation via the YXXQ motif-derived signal. Furthermore, this study revealed a novel role for STAT3 in IL-6-induced NLK activation but not in TGFβ-induced NLK activation. STAT3 functions as a scaffold for TAK1 and NLK specifically in IL-6 signaling by binding them at its carboxyl-terminal region. The following observations support the idea that this interaction is physiologically significant: (i) most TAK1-NLK interactions in the nuclear extracts of IL-6-stimulated HepG2 cells depended on the presence of STAT3 (Fig. 5B ); (ii) the IL-6-induced NLK activation was greatly decreased in HepG2-STAT3KD cells; (iii) STAT3 and TAK1 were independently activated by IL-6, even at low concentrations, and they then translocated into the nucleus (Figs. 4B ...
View Notes - Stat841f09 - Wiki Course Notes from STAT 441/8 stat 441/8 at University of Waterloo, Waterloo. 10/09/2013 Stat841 - Wiki Cour se Notes Stat841 From Wiki Cours e Notes Contents 1
кДНК STAT3 была впервые клонирована в 1994 году под именем APRF (англ. acute-phase response factor)[2]. В 1996 году была открыта укороченная изоформа мРНК STAT3, которая образуется в результате альтернативного сплайсинга. В этой мРНК отсутствует фрагмент длиной около 50 нуклеотидов, соответствующая изоформа белка называется STAT3β и является негативным регулятором транскрипции[3].. Полноразмерный белок STAT3α состоит из 770 аминокислотных остатков и имеет молекулярную массу около 92 кДа. Изоформа STAT3β имеет молекулярную массу около 80 кДа[4].. STAT3 имеет типичную для всех STAT-белков ...
STAT6 is a member of the STAT family of transcription factors. In response to cytokines and growth factors, STAT family members are phosphorylated by…
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Clone REA324 recognizes the signal transducer and activator of transcription 3 (STAT3) antigen phosphorylated at serine 727 (pS727). STAT3 expression is found ubiquitously. It is activated in response to various growth factors, hormones, and cytokines, and has an important role in their signaling. When these ligands bind to the specific transmembrane STAT3 receptor, STAT3 becomes activated by tyrosine phosphorylation of two important phosphorylation sites, pY705 and pS727. The dimeric STAT3 translocates to the nucleus, where it binds to consensus STAT3 binding sequences within the promoter region of target genes and thereby activates their transcription. The persistent activation of STAT3 also mediates tumor-promoting inflammation. STAT3 promotes pro-oncogenic inflammatory pathways in tumor inflammation and immunity, including nuclear factor-κB and interleukin-6-GP130-Janus kinase pathways, and by opposing STAT1- and NF-κB-mediated T helper 1 anti-tumor immune responses. Additional information: Clone
Despite evidence implicating transcription factors, including STAT3, in oncogenesis, these proteins have been regarded as "undruggable." We developed a decoy targeting STAT3 and conducted a phase 0 trial. Expression levels of STAT3 target genes were decreased in head and neck cancers following injection with the STAT3 decoy compared with tumors receiving saline control. Decoys have not been amenable to systemic administration due to instability. To overcome this barrier, we linked the oligonucleotide strands using hexaethylene glycol spacers. This cyclic STAT3 decoy bound with high affinity to STAT3 protein, reduced cellular viability, and suppressed STAT3 target gene expression in cancer cells. Intravenous injection of the cyclic STAT3 decoy inhibited xenograft growth and downregulated STAT3 target genes in the tumors. These results provide the first demonstration of a successful strategy to inhibit tumor STAT3 signaling via systemic administration of a selective STAT3 inhibitor, thereby paving ...
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siRNA mediated knockdown of STAT3. A. Histogram of STAT3 levels in SW480 colon carcinoma cells treated with STAT3 and NTC (non-targeting) siRNAs. Red bars denot
Rabbit anti STAT4 (pTyr693) antibody recognizes STAT4 when phosphorylated at tyrosine 693. STAT4 is a member of the STAT4 family of transc
Pub. L. 92-573, 86 Stat. 1207 (15 U.S.C. 2051-81) as amended by Pub. L. 94-284, 90 Stat. 503, Pub. L. 95-319, 92 Stat. 386, Pub. L. 95-631, 92 Stat. 3742; Pub. L. 90-189, 81 Stat. 568 (15 U.S.C. 1191-1204); Pub. L. 86-613, 74 Stat. 372, as amended by Pub. L. 89-756, 80 Stat. 1303, and Pub. L. 91-113, 83 Stat. 187 (15 U.S.C. 1261-74); Pub. L. 91-601, 84 Stat. 1670 (15 U.S.C. 1471-76) and the Act of Aug. 7, 1956, 70 Stat. 953 (15 U.S.C. 1211-14 ...
Here is the best resource for homework help with STAT 211 : Stat 1 at Rutgers. Find STAT211 study guides, notes, and practice tests from Rutgers.
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Complete information for STAT2 gene (Protein Coding), Signal Transducer And Activator Of Transcription 2, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
... , Authors: Amanda M Del Rosario, Teresa M Bernaciak, Corinne M Silva. Published in: Atlas Genet Cytogenet Oncol Haematol.
EML4-ALK was only recently identified as a transforming fusion gene in NSCLC (4). Although EML4-ALK was shown to possess marked oncogenic activity both in vitro and in vivo (4, 15), the signaling pathways underlying malignant transformation by the fusion protein have remained unclear. We have now shown that phosphorylation of both ERK and STAT3 was similarly and markedly increased in NIH 3T3 cells by forced expression of either variant 1 or variant 3 of EML4-ALK, whereas phosphorylation of AKT remained unaffected. Similar effects were observed in different clones of these cells stably transfected with a vector for either variant of EML4-ALK (data not shown). We further showed that the growth of both 3T3/EAV1 and 3T3/EAV3 cells was significantly attenuated by inhibition of ERK or STAT3 signaling but not by that of PI3K signaling. NPM-ALK has also been shown to activate ERK and STAT3 signaling pathways (6, 27-33), both of which are thought to be essential downstream mediators of the oncogenic ...
Ver, regardless of whether STAT3 inhibition can make improvements to our good results in dealing with 1365888-06-7 Biological Activity breast most cancers continues to be being studied in long run studies. On top of that, STAT5 and STAT3 mediate opposing consequences on several crucial concentrate on genes in breast cancer cells, with STAT5 exerting a dominant job [37]. It might have an interest to examine what is the status of STAT5 in breast most cancers stem-like cells.Supporting InformationFigure SThe synthesis of LLL12.(JPG)Figure S2 LLL12 52328-98-0 Epigenetic Reader Domain inhibited STAT3 phosphorylation, and down-regulated STAT3-regulated genes, Cyclin D1, Survivin, Bcl-2 and Twist1, also as induced apoptosis in un-seperated MDA-MB-231, SK-BR-3, and SUM159 breast cancer cells. LLL12 was synthesized in Dr. Pui-Kai Lis laboratory (College of Pharmacy, The Ohio Point out College). Unseparated cells were being addressed with ten mM of LLL12 or DMSO for 24 hrs, plus the phosphorylation of ...
The Ac2-26-mediated STAT3 activation is JAK-dependent and induces nuclear translocation and DNA binding of phosphorylated STAT3 as well as increased SOCS3 expre
Jo Schmo reist durch die Zeit - Die lauteste Rülps-Attacke der Welt Keine Schurken weit und breit. Seit der irreböse Dr. Garstigg hinter Gittern ist, ist Jo Schmo, Grundschul-Superheldin, einfach nur LANGWEILIG. Da kommt ihr eine super Idee - vielleicht kann sie ja in der Vergangenheit ein paar böse Jungs jagen! Und noch während Jo an einer Zeitmaschine baut, ahnt sie nicht, dass sich direkt unter ihrer Superheldennase eine klitzekleine Verbrechenswelle zusammenbraut ... und damit ein Abenteuer für Jo! Gebundene Ausgabe: 120 SeitenVerlag: ArenaEmpfohlenes Alter: 8 - 10 Jahre
Jo Schmo reist durch die Zeit - Die lauteste Rülps-Attacke der Welt Keine Schurken weit und breit. Seit der irreböse Dr. Garstigg hinter Gittern ist, ist Jo Schmo, Grundschul-Superheldin, einfach nur LANGWEILIG. Da kommt ihr eine super Idee - vielleicht kann sie ja in der Vergangenheit ein paar böse Jungs jagen! Und noch während Jo an einer Zeitmaschine baut, ahnt sie nicht, dass sich direkt unter ihrer Superheldennase eine klitzekleine Verbrechenswelle zusammenbraut ... und damit ein Abenteuer für Jo! Gebundene Ausgabe: 120 SeitenVerlag: ArenaEmpfohlenes Alter: 8 - 10 Jahre
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STAT5-Interacting Proteins: A Synopsis of Proteins that Regulate STAT5 Activity. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Version 9.1 online documentation for SAS To get documentation on statistical PROCs, click on the + next to SAS/STAT, then the + next to SAS/STAT Users Guide. After a short wait, youll get a list of all the PROCs in SAS/STAT. Click the + next to the desired procedure for more information. The syntax section is usually the most helpful to find errors. Other sections provide advice on interpretation. < ...
The AlphaLISA® SureFire® Ultra™ p-STAT4 (Tyr693) assay kit is an immunoassay for quantitative detection of endogenous STAT4 (phosphorylated at Tyr693) in cellular lysates.
Reagents. Sunitinib (SU11248; Sutent) was purchased from City of Hope Medical Center Pharmacy. Human Stat3 small interfering RNA (siRNA), control siRNA, anti-Stat3 (C-20), anti-Bcl-xL (H-5), anti-survivin (D-8), anti-HDAC1 (H-11), and anti-poly(ADP-ribose) polymerase (PARP) were obtained from Santa Cruz Biotechnology; anti-cyclin E (clone HE12) was from BD Biosciences; anti-cyclin D1 (AB-3) and anti-Bcl-2 were from Calbiochem; anti-β-actin (AC-74) was from Sigma; and anti-phosphorylated Stat3 (p-Stat3; Tyr705), anti-phosphorylated Src (p-Src; Tyr416)/anti-Src, anti-phosphorylated AKT (p-AKT; Ser473)/anti-AKT, anti-phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2; Thr202/Tyr204)/anti-ERK1/2, and anti-phosphorylated Janus-activated kinase 2 (p-JAK2; Tyr1007/1008)/anti-JAK2 were from Cell Signaling Technology, Inc. FITC-conjugated, phycoerythrin-conjugated, or allophycocyanin (APC)-conjugated monoclonal antibodies to mouse CD4, CD8, CD11b, CD11c, Gr1, and phosphotyrosine-Stat3 ...
Sehr geehrte Forrester-Kunden, Softwareanbieter, Forrester-Kollegen und Freunde,. Persönliche Karrieren ähneln in gewisser Weise Innovationen in der Technologiebranche: Sie nehmen eine Herausforderung an, bringen neue Ideen ein, erreichen einige Ziele und verbessern sich dann über Jahre hinweg kontinuierlich. Sie arbeiten seit vielen Jahren in der technologischen Innovation und kennen Konzepte wie das "Innovators Dilemma". Sie können sich vorstellen, dass auch persönliche Karrieren manchmal eine störende Veränderung erfordern. Nach sieben erstaunlichen Jahren beschloss ich, Forrester Research bis zum 17. Dezember zu verlassen. Jetzt werde ich bei anwalt für familienrecht deggendorf arbeiten, wo sie gute Rechtsberatung bieten. Sie sind das beste verfügbare Rechtsteam. Danke für alles.. Das Unternehmen ist seit vielen Jahren ein Anbieter von Ral Farben online bestellen, hat sich nun aber seit rund zwei Jahrzehnten auf Schulausflüge, Exkursionen, Schulausflüge oder Studienreisen ...
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View mouse Stat6 Chr10:127642986-127660957 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression
Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.
We have professional and advanced research and production capacity for STAT6 reagents production, including Proteins, Antibodies, cDNA Clones,etc. All STAT6 products are produced in house and quality controlled.