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https://www.readbyqxmd.com/read/28634859/erratum-to-erythropoietin-rescues-memory-impairment-in-a-rat-model-of-chronic-cerebral-hypoperfusion-via-the-epo-r-jak2-stat5-pi3k-akt-gsk-3%C3%AE-pathway
#1
Shengli Ma, Juwu Chen, Chen Chen, Na Wei, Jingjing Xu, Guohui Yang, Nan Wang, Yu Meng, Jia Ren, Zongchao Xu
No abstract text is available yet for this article.
June 20, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28631564/indole-3-carbinol-induces-apoptosis-of-chronic-myelogenous-leukemia-cells-through-suppression-of-stat5-and-akt-signaling-pathways
#2
Majid Safa, Leila Jafari, Fatemeh Alikarami, Rima Manafi Shabestari, Ahmad Kazemi
Signal transducer and activator of transcription 5 and Akt pathways, implicated in signaling transduction downstream of BCR-ABL, play critical roles in the pathogenesis of chronic myeloid leukemia. Therefore, idenication of novel compounds that modulate the activity of such pathways could be a new approach in the treatment of chronic myeloid leukemia. Previous studies have demonstrated that indole-3-carbinol inhibits the proliferation and induces apoptosis of various tumor cells. However, its anticancer activity against chronic myeloid leukemia cells and the underlying mechanism remain unclear...
June 2017: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
https://www.readbyqxmd.com/read/28629526/erythropoietin-receptor-signaling-and-lipid-rafts
#3
Kathy McGraw, Alan List
Erythropoiesis is tightly regulated by the growth factor erythropoietin (Epo). Signal activation begins when Epo engages its cognate receptor, Epo-R, triggering receptor homodimerization, and recruitment of signaling intermediates including Jak2 that phosphorylates both the receptor cytoplasmic tail and downstream effectors including the transcription factor, STAT5. Transcription factors subsequently activate transcription of prosurvival and prodifferentiation genes responsible for red blood cell production...
2017: Vitamins and Hormones
https://www.readbyqxmd.com/read/28629523/significance-of-erythropoietin-receptor-antagonist-emp9-in-cancers
#4
Yoshiko Yasuda, Mitsugu Fujita
We have clarified that cancer cells express their own erythropoietin (Epo) and its receptor (EpoR) mRNA levels, and the respective proteins, which are under the control of Epo-EpoR signaling. Then we explored to inhibit the Epo-EpoR signaling with an EpoR antagonist Epo mimetic peptide 9 (EMP9) that is a derivative of an Epo-mimicking peptide EMP1. In the study of the cancer cell lines in vitro, rhEpo accelerated the cancer cell growth, whereas the EMP9 inhibited the cell growth along with the inhibition of STAT5 tyrosine phosphorylation...
2017: Vitamins and Hormones
https://www.readbyqxmd.com/read/28622305/the-thrombopoietin-mpl-axis-is-activated-in-the-gata1-low-mouse-model-of-myelofibrosis-and-is-associated-with-a-defective-rps14-signature
#5
M Zingariello, L Sancillo, F Martelli, F Ciaffoni, M Marra, L Varricchio, R A Rana, C Zhao, J D Crispino, A R Migliaccio
Myelofibrosis (MF) is characterized by hyperactivation of thrombopoietin (TPO) signaling, which induces a RPS14 deficiency that de-regulates GATA1 in megakaryocytes by hampering its mRNA translation. As mice carrying the hypomorphic Gata1(low) mutation, which reduces the levels of Gata1 mRNA in megakaryocytes, develop MF, we investigated whether the TPO axis is hyperactive in this model. Gata1(low) mice contained two times more Tpo mRNA in liver and TPO in plasma than wild-type littermates. Furthermore, Gata1(low) LSKs expressed levels of Mpl mRNA (five times greater than normal) and protein (two times lower than normal) similar to those expressed by LSKs from TPO-treated wild-type mice...
June 16, 2017: Blood Cancer Journal
https://www.readbyqxmd.com/read/28606561/stat5-deletion-in-macrophages-alters-ductal-elongation-and-branching-during-mammary-gland-development
#6
Nicholas J Brady, Michael A Farrar, Kathryn L Schwertfeger
Macrophages are required for proper mammary gland development and maintaining tissue homeostasis. However, the mechanisms by which macrophages regulate this process remain unclear. Here, we identify STAT5 as an important regulator of macrophage function in the developing mammary gland. Analysis of mammary glands from mice with STAT5-deficient macrophages demonstrates delayed ductal elongation, enhanced ductal branching and increased epithelial proliferation. Further analysis reveals that STAT5 deletion in macrophages leads to enhanced expression of proliferative factors such as Cyp19a1/aromatase and IL-6...
June 9, 2017: Developmental Biology
https://www.readbyqxmd.com/read/28605125/isoflavones-and-their-metabolites-influence-the-milk-component-synthesis-ability-of-mammary-epithelial-cells-through-prolactin-stat5-signaling
#7
Yusaku Tsugami, Kota Matsunaga, Takahiro Suzuki, Takanori Nishimura, Ken Kobayashi
SCOPE: Isoflavones are a class of polyphonic compounds present in legumes and are called phytoestrogens because of their estrogen-like activity. Estrogen influences the behavior of mammary epithelial cells (MECs) during pregnancy and lactation. In this study, we investigated the direct influences of isoflavones and their metabolites in milk production ability of MECs. METHODS AND RESULTS: Mouse MECs were cultured with prolactin and dexamethasone (glucocorticoid analog) to induce milk production ability...
June 12, 2017: Molecular Nutrition & Food Research
https://www.readbyqxmd.com/read/28600954/high-throughput-thermofluor-based-assays-for-inhibitor-screening-of-stat-sh2-domains
#8
Elvin D de Araujo, Pimyupa Manaswiyoungkul, Johan Israelian, Jisung Park, Karen Yuen, Shiva Farhangi, Angelika Berger-Becvar, Lubna Abu-Jazar, Patrick T Gunning
The development of STAT protein-specific inhibitors has been the focus of a number of drug discovery programs. STAT activation occurs through phosphorylation at the STAT SH2 domain, resulting in dimerization, translocation to the nucleus, and transcription of proliferative genes. Due to the functional significance of the SH2 domain in mediating multiple components of the STAT signalling cascade, many libraries of inhibitors have been designed to target the SH2 domain. This has triggered the requirement for effective high-throughput screening platforms for analyzing binding by larger chemical libraries to STAT proteins...
May 1, 2017: Journal of Pharmaceutical and Biomedical Analysis
https://www.readbyqxmd.com/read/28598969/cucurbitacin-e-reduces-obesity-and-related-metabolic-dysfunction-in-mice-by-targeting-jak-stat5-signaling-pathway
#9
Munazza Murtaza, Gulnaz Khan, Meha Fatima Aftab, Shabbir Khan Afridi, Safina Ghaffar, Ayaz Ahmed, Rahman M Hafizur, Rizwana Sanaullah Waraich
Several members of cucurbitaceae family have been reported to regulate growth of cancer by interfering with STAT3 signaling. In the present study, we investigated the unique role and molecular mechanism of cucurbitacins (Cucs) in reducing symptoms of metabolic syndrome in mice. Cucurbitacin E (CuE) was found to reduce adipogenesis in murine adipocytes. CuE treatment diminished hypertrophy of adipocytes, visceral obesity and lipogenesis gene expression in diet induced mice model of metabolic syndrome (MetS)...
2017: PloS One
https://www.readbyqxmd.com/read/28596283/combined-targeting-of-stat3-and-stat5-a-novel-approach-to-overcome-drug-resistance-in-chronic-myeloid-leukemia
#10
Karoline V Gleixner, Mathias Schneeweiss, Gregor Eisenwort, Daniela Berger, Harald Herrmann, Katharina Blatt, Georg Greiner, Konstantin Byrgazov, Gregor Hoermann, Marina Konopleva, Islam Waliul, Abbarna A Cumaraswamy, Patrick T Gunning, Hiroshi Maeda, Richard Moriggl, Michael Deininger, Thomas Lion, Michael Andreeff, Peter Valent
In chronic myeloid leukemia, resistance against BCR-ABL1 tyrosine kinase inhibitors can develop because of BCR-ABL1 mutations, activation of additional pro-oncogenic pathways, and stem cell resistance. Drug combinations covering a broad range of targets may overcome resistance. CDDO-Me is a drug that inhibits the survival of leukemic cells by targeting different pro-survival molecules, including STAT3. We found that CDDO-Me inhibits proliferation and survival of tyrosine kinase inhibitor-resistant BCR-ABL1+ cell lines and primary leukemic cells, including cells harboring BCR-ABL1T315I or T315I+ compound mutations...
June 8, 2017: Haematologica
https://www.readbyqxmd.com/read/28595903/shc004-221a1-a-novel-tyrosine-kinase-potently-inhibits-t315i-mutant-bcr-abl-in-chronic-myeloid-leukemia
#11
Duowei Wang, Yan Zheng, Jiaying Li, Hongxi Wu, Xianjing Li, Ying Tang, Yang Liu, Jiani Li, Rui Sun, Youli Zhou, Jihong Sun, Yong Yang
Although judicious use of tyrosine kinase inhibitors that target BCR-ABL constitutes an effective strategy for the control of chronic myeloid leukemia (CML), drug resistance is observed due to kinase domain mutations, among which a major one is BCR-ABL(T315I). In this study, we identified SHC004-221A1 as a potent inhibitor of T315I and other BCR-ABL mutants. Biochemical assays demonstrated that SHC004-221A1 has an inhibitory effect on all selected BCR-ABL mutants. In vitro studies showed that SHC004-221A1 inhibited the proliferation of tumor cell lines carrying native and T315I mutant BCR-ABL...
June 5, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28588262/identification-of-new-shikonin-derivatives-as-antitumor-agents-targeting-stat3-sh2-domain
#12
Han-Yue Qiu, Xiang Zhu, Yue-Lin Luo, Hong-Yan Lin, Cheng-Yi Tang, Jin-Liang Qi, Yan-Jun Pang, Rong-Wu Yang, Gui-Hua Lu, Xiao-Ming Wang, Yong-Hua Yang
Signal transducer and activator of transcription 3 (STAT3) is hyper-activated in diversiform human tumors and has been validated as an attractive therapeutic target. Current research showed that a natural product, shikonin, along with its synthetic analogues, is able to inhibit the activity of STAT3 potently. The potential space of shikonin in developing novel anti-cancer agents encouraged us to carry out the investigation of the probable binding mode with STAT3. From this foundation, we have designed new types of STAT3 SH2 inhibitors...
June 6, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28586756/inhibitors-of-the-pi3k-mtor-pathway-prevent-stat5-phosphorylation-in-jak2v617f-mutated-cells-through-pp2a-cip2a-axis
#13
Niccol├▓ Bartalucci, Laura Calabresi, Manjola Balliu, Serena Martinelli, Maria Caterina Rossi, Jean Luc Villeval, Francesco Annunziato, Paola Guglielmelli, Alessandro M Vannucchi
Inhibition of the constitutively activated JAK/STAT pathway in JAK2V617F mutated cells by the JAK1/JAK2 inhibitor ruxolitinib resulted in clinical benefits in patients with myeloproliferative neoplasms. However, evidence of disease-modifying effects remains scanty; furthermore, some patients do not respond adequately to ruxolitinib, or have transient responses, thus novel treatment strategies are needed. Here we demonstrate that ruxolitinib causes incomplete inhibition of STAT5 in JAK2V617F mutated cells due to persistence of phosphorylated serine residues of STAT5b, that conversely are targeted by PI3K and mTORC1 inhibitors...
May 22, 2017: Oncotarget
https://www.readbyqxmd.com/read/28582466/aberrant-plasma-il-7-and-soluble-il-7-receptor-levels-indicate-impaired-t-cell-response-to-il-7-in-human-tuberculosis
#14
Christian Lundtoft, Anthony Afum-Adjei Awuah, Jens Rimpler, Kirstin Harling, Norman Nausch, Malte Kohns, Ernest Adankwah, Franziska Lang, Laura Olbrich, Ertan Mayatepek, Ellis Owusu-Dabo, Marc Jacobsen
T-cell proliferation and generation of protective memory during chronic infections depend on Interleukin-7 (IL-7) availability and receptivity. Regulation of IL-7 receptor (IL-7R) expression and signalling are key for IL-7-modulated T-cell functions. Aberrant expression of soluble (s) and membrane-associated (m) IL-7R molecules is associated with development of autoimmunity and immune failure in acquired immune deficiency syndrome (AIDS) patients. Here we investigated the role of IL-7/IL-7R on T-cell immunity in human tuberculosis...
June 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28576744/jak-stat-signaling-and-cancer-opportunities-benefits-and-side-effects-of-targeted-inhibition
#15
REVIEW
Bernd Groner, Viktoria von Manstein
The effects of Jak Stat signaling and the persistent activation of Stat3 and Stat5 on tumor cell survival, proliferation and invasion have made the Jak Stat pathway a favorite target for drug development and cancer therapy. This notion was strengthened when additional biological functions of Stat signaling in cancer and their roles in the regulation of cytokine dependent inflammation and immunity in the tumor microenvironment were discovered. Stats act not only as transcriptional inducers, but affect gene expression via epigenetic modifications, induce epithelial mesenchymal transition, generate a pro-tumorigenic microenvironment, promote cancer stem cell self-renewal and differentiation, and help to establish the pre-metastatic niche formation...
May 30, 2017: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/28556300/development-of-protein-degradation-inducers-of-oncogenic-bcr-abl-protein-by-conjugation-of-abl-kinase-inhibitors-and-iap-ligands
#16
Norihito Shibata, Naoki Miyamoto, Katsunori Nagai, Kenichiro Shimokawa, Tomoya Sameshima, Nobumichi Ohoka, Takayuki Hattori, Yasuhiro Imaeda, Hiroshi Nara, Nobuo Cho, Mikihiko Naito
Chromosomal translocation occurs in some cancer cells, which results in the expression of aberrant oncogenic fusion proteins that include BCR-ABL in chronic myelogenous leukemia (CML). Inhibitors of ABL tyrosine kinase such as imatinib and dasatinib exhibit remarkable therapeutic effects, though emergence of drug resistance hampers the therapy during long-term treatment. An alternative approach to treat CML is to down-regulate the BCR-ABL protein. We have devised a protein knockdown system by hybrid molecules named SNIPERs (Specific and Non-genetic inhibitor of apoptosis protein [IAP]-dependent Protein Erasers), which is designed to induce IAP-mediated ubiquitylation and proteasomal degradation of target proteins, and a couple of SNIPER(ABL) against BCR-ABL protein has been developed recently...
May 26, 2017: Cancer Science
https://www.readbyqxmd.com/read/28555080/deregulation-of-kinase-signaling-and-lymphoid-development-in-ebf1-pdgfrb-all-leukemogenesis
#17
S J Welsh, M L Churchman, M Togni, C G Mullighan, J Hagman
The chimeric fusion oncogene EBF1-PDGFRB is a recurrent lesion observed in Ph-like B-ALL and is associated with particularly poor prognosis. While it is understood that this fusion activates tyrosine kinase signaling, the mechanisms of transformation and importance of perturbation of EBF1 activity remain unknown. EBF1 is a nuclear transcription factor required for normal B-lineage specification, commitment, and development. Conversely, PDGFRB is a receptor tyrosine kinase that is normally repressed in lymphocytes, yet PDGFRB remains a common fusion partner in leukemias...
May 30, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28551085/bi-directionally-protective-communication-between-neurons-and-astrocytes-under-ischemia
#18
Xiao-Mei Wu, Christopher Qian, Yu-Fu Zhou, Yick-Chun Yan, Qian-Qian Luo, Wing-Ho Yung, Fa-Li Zhang, Li-Rong Jiang, Zhong Ming Qian, Ya Ke
The extensive existing knowledge on bi-directional communication between astrocytes and neurons led us to hypothesize that not only ischemia-preconditioned (IP) astrocytes can protect neurons but also IP neurons protect astrocytes from lethal ischemic injury. Here, we demonstrated for the first time that neurons have a significant role in protecting astrocytes from ischemic injury. The cultured medium from IP neurons (IPcNCM) induced a remarkable reduction in LDH and an increase in cell viability in ischemic astrocytes in vitro...
May 20, 2017: Redox Biology
https://www.readbyqxmd.com/read/28549597/prolactin-receptor-targeting-in-breast-and-prostate-cancers-new-insights-into-an-old-challenge
#19
REVIEW
Vincent Goffin
In the era of precision medicine, the identification of new targets is a constant challenge to improve cancer therapy. Preclinical investigations, epidemiological studies and analyses of tissue specimens from patients strongly support the contribution of prolactin receptor (PRLR) signaling to breast and prostate tumorigenesis and cancer progression. Although a clear causative link with mutations of the genes encoding prolactin or its receptor is lacking, increased PRLR signaling in these cancers can be assessed by the overexpression of cognate proteins and is often confirmed by over-activation of downstream signaling effectors...
May 23, 2017: Pharmacology & Therapeutics
https://www.readbyqxmd.com/read/28528355/increased-retinol-free-rbp4-contributes-to-insulin-resistance-in-gestational-diabetes-mellitus
#20
Yanmin Chen, Ping Lv, Mengkai Du, Zhaoxia Liang, Menglin Zhou, Danqing Chen
PURPOSE: Retinol-binding protein 4 (RBP4) is a circulating retinol transporter that is strongly associated with insulin resistance. The aim of this study was to evaluate the RBP4 and retinol level in rat model of gestational diabetes mellitus and the relationship between retinol-free RBP4 (apo-RBP4), retinol-bound RBP4 (holo-RBP4) and insulin resistance. METHODS: Pregnant rats were administered streptozotocin to induce diabetes. The RBP4 and retinol levels were evaluated in GDM and normal pregnant rats...
May 20, 2017: Archives of Gynecology and Obstetrics
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