scholarly journals Mutational Evidence for the Critical Role of CBF Transcription Factors in Cold Acclimation in Arabidopsis

2016 ◽  
Vol 171 (4) ◽  
pp. 2744-2759 ◽  
Author(s):  
Chunzhao Zhao ◽  
Zhengjing Zhang ◽  
Shaojun Xie ◽  
Tong Si ◽  
Yuanya Li ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Cold Acclimation ◽  
Critical Role ◽  
Cbf Transcription Factors

scholarly journals Megakaryopoiesis and Platelet Biology: Roles of Transcription Factors and Emerging Clinical Implications

2021 ◽  
Vol 22 (17) ◽  
pp. 9615
Author(s):  
Ji-Yoon Noh
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Transcription Factors ◽  
Blood Cells ◽  
Thrombus Formation ◽  
Critical Role ◽  
Clinical Implications ◽  
Disease Development ◽  
Hematopoietic Stem

Platelets play a critical role in hemostasis and thrombus formation. Platelets are small, anucleate, and short-lived blood cells that are produced by the large, polyploid, and hematopoietic stem cell (HSC)-derived megakaryocytes in bone marrow. Approximately 3000 platelets are released from one megakaryocyte, and thus, it is important to understand the physiologically relevant mechanism of development of mature megakaryocytes. Many genes, including several key transcription factors, have been shown to be crucial for platelet biogenesis. Mutations in these genes can perturb megakaryopoiesis or thrombopoiesis, resulting in thrombocytopenia. Metabolic changes owing to inflammation, ageing, or diseases such as cancer, in which platelets play crucial roles in disease development, can also affect platelet biogenesis. In this review, I describe the characteristics of platelets and megakaryocytes in terms of their differentiation processes. The role of several critical transcription factors have been discussed to better understand the changes in platelet biogenesis that occur during disease or ageing.

scholarly journals Hypoxic Regulation of Neutrophils in Cancer

2019 ◽  
Vol 20 (17) ◽  
pp. 4189 ◽  
Author(s):  
Daniel Triner ◽  
Yatrik M. Shah
Keyword(s):  
Transcription Factors ◽  
Therapeutic Target ◽  
Human Cancer ◽  
Critical Role ◽  
Neutrophil Function ◽  
Neoplastic Progression ◽  
Specific Expression ◽  
Microbial Response ◽  
Novel Therapeutic

Neutrophils have been well-characterized for their role in the host anti-microbial response. However, it is now appreciated that neutrophils have a critical role in tumorigenesis and tumor progression in the majority of solid tumors. Recent studies have indicated a critical role for hypoxia in regulating neutrophil function in tumors. Furthermore, neutrophil-specific expression of hypoxia-inducible transcription factors may represent a novel therapeutic target for human cancer. In this review, we highlight the function of neutrophils in cancer and the role of the neutrophil hypoxic response in regulating the neoplastic progression of cancer.

FoxO3 transcription factor promotes autophagy after oxidative stress injury in HT22 cells

2020 ◽  
Author(s):  
Aiqing Deng ◽  
Limin Ma ◽  
Xueli Zhou ◽  
Xin Wang ◽  
Shouyan Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factors ◽  
Cell Injury ◽  
Cell Damage ◽  
Critical Role ◽  
Neuronal Cell ◽  
Ht22 Cells ◽  
Stress Injury ◽  
Oxidative Stress Injury

Autophagy has been implicated in neurodegenerative diseases. Forkhead box O3 (FoxO3) transcription factors promote autophagy in heart and inhibit oxidative damage. Here we investigate the role of FoxO3 transcription factors in regulating autophagy after oxidative stress injury in immortalized mouse hippocampal cell line (HT22). The present study confirms that hydrogen peroxide (H2O2) injury could induce autophagy and FoxO3 activation in HT22 cells. In addition, overexpression of FoxO3 enhanced H2O2-induced autophagy activation and suppressed neuronal cell damage, while knockdown of FoxO3 reduced H2O2-induced autophagy activation and exacerbated neuronal cell injury. Inhibition of autophagy by 3-Methyladenine (3-MA) resulted in reduced cell viability, increased production of reactive oxygen species (ROS), promoted nuclear condensation and decreased expression of antiapoptotic and autophagy-related proteins, indicating that autophagy may have protective effects on H2O2-induced injury in HT22 cells. Moreover, overexpression of FoxO3 prevented exacerbation of brain damage induced by 3-MA. Taken together, these results show that activation of FoxO3 could induce autophagy and inhibit H2O2-induced damage in HT22 cells. Our study demonstrates the critical role of FoxO3 in regulating autophagy in brain.

scholarly journals Postnatal Body Growth Is Dependent on the Transcription Factors Signal Transducers and Activators of Transcription 5a/b in Muscle: A Role for Autocrine/Paracrine Insulin-Like Growth Factor I

Endocrinology ◽  
2007 ◽  
Vol 148 (4) ◽  
pp. 1489-1497 ◽  
Author(s):  
Peter Klover ◽  
Lothar Hennighausen
Keyword(s):  
Skeletal Muscle ◽  
Transcription Factors ◽  
Critical Role ◽  
Postnatal Growth ◽  
Growth Defect ◽  
Mrna Levels ◽  
Signal Transducers ◽  
Igf I ◽  
Signal Transducers And Activators

The transcription factors signal transducers and activators of transcription (STAT)5a and STAT5b (STAT5) are essential mediators of many actions of GH, including transcription of the IGF-I gene. Here, we present evidence that skeletal muscle STAT5 is important for postnatal growth and suggest that this is conveyed by the production of localized IGF-I. To investigate the role of STAT5 signaling in skeletal muscle, mice with a skeletal-muscle-specific deletion of the Stat5a and Stat5b genes (Stat5MKO mice) were used. IGF-I mRNA levels were reduced by 60% in muscle tissue of these mice. Despite only a 15% decrease in circulating IGF-I, 8-wk-old male Stat5MKO mice displayed approximately 20% reduction in body weight that was accounted for by a reduction in lean mass. The skeletons of Stat5MKO mice were found to be smaller than controls, indicating the growth defect was not restricted to skeletal muscle. These results demonstrate an as yet unreported critical role for STAT5 in skeletal muscle for local IGF-I production and postnatal growth and suggest the skeletal muscle as a major site of GH action.

scholarly journals Role of CBF transcription factors during long-term acclimation to high light and low temperature in two ecotypes of a winter annual

2020 ◽  
Author(s):  
christopher baker ◽  
Jared Stewart ◽  
Cynthia Amstutz ◽  
Jeffrey Johnson ◽  
Lindsey Ching ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Low Temperature ◽  
High Light ◽  
Winter Annual ◽  
Cbf Transcription Factors

scholarly journals Double knock-out of Hmga1 and Hipk2 genes causes perinatal death associated to respiratory distress and thyroid abnormalities in mice

2019 ◽  
Vol 10 (10) ◽  
Author(s):  
Raffaele Gerlini ◽  
Elena Amendola ◽  
Andrea Conte ◽  
Valeria Valente ◽  
Mara Tornincasa ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Perinatal Death ◽  
Critical Role ◽  
Surfactant Proteins ◽  
Drastic Reduction ◽  
Differentiation Markers ◽  
Altered Expression ◽  
Knock Out

Abstract The serine–threonine kinase homeodomain-interacting protein kinase 2 (HIPK2) modulates important cellular functions during development, acting as a signal integrator of a wide variety of stress signals, and as a regulator of transcription factors and cofactors. We have previously demonstrated that HIPK2 binds and phosphorylates High-Mobility Group A1 (HMGA1), an architectural chromatinic protein ubiquitously expressed in embryonic tissues, decreasing its binding affinity to DNA. To better define the functional role of HIPK2 and HMGA1 interaction in vivo, we generated mice in which both genes are disrupted. About 50% of these Hmga1/Hipk2 double knock-out (DKO) mice die within 12 h of life (P1) for respiratory failure. The DKO mice present an altered lung morphology, likely owing to a drastic reduction in the expression of surfactant proteins, that are required for lung development. Consistently, we report that both HMGA1 and HIPK2 proteins positively regulate the transcriptional activity of the genes encoding the surfactant proteins. Moreover, these mice display an altered expression of thyroid differentiation markers, reasonably because of a drastic reduction in the expression of the thyroid-specific transcription factors PAX8 and FOXE1, which we demonstrate here to be positively regulated by HMGA1 and HIPK2. Therefore, these data indicate a critical role of HIPK2/HMGA1 cooperation in lung and thyroid development and function, suggesting the potential involvement of their impairment in the pathogenesis of human lung and thyroid diseases.

scholarly journals The Emerging Role of Inhibitor of Growth 4 as a Tumor Suppressor in Multiple Human Cancers

2015 ◽  
Vol 36 (2) ◽  
pp. 409-422 ◽  
Author(s):  
Shiyun Cui ◽  
Yanping Gao ◽  
Kai Zhang ◽  
Jing Chen ◽  
Rui Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Transcription Factors ◽  
Tumor Suppressor ◽  
Gene Deletion ◽  
Critical Role ◽  
Chromatin Modification ◽  
Transcriptional Dysregulation ◽  
Tumorigenesis And Progression ◽  
Nf Kappab

Inhibitor of growth 4 (ING4), a member of the conserved ING family, has been identified as an important tumor suppressor since it plays a critical role in the regulation of chromatin modification, cell proliferation, angiogenesis and cell migration. Some observations suggest that ING4 acts as a key regulator of tumorigenesis through modifying gene transcription in part by regulating the transcription factors p53 and NF-kappaB (NF-κB). However, these models have yet to be substantiated by further investigations. Numerous reports describe the reduced expression of ING4 in cancers, and the responsible mechanisms are involved in gene deletion, mutation, transcriptional and post-transcriptional dysregulation. This review aims to summarize the recent published literature that investigates the role of ING4 in regulating tumorigenesis and progression, and explore its potential for cancer treatment.

The Promise of Epigenetics. Has It Delivered New Insights?

2016 ◽  
Vol 34 (1-2) ◽  
pp. 12-19 ◽  
Author(s):  
Judy H. Cho
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Disease Prevention ◽  
Critical Role ◽  
Mononuclear Phagocytes ◽  
T Cell Subsets ◽  
Cd4 T Cell ◽  
Specific Gene ◽  
Interleukin 23

Enrichment of GWAS signals within cell-specific enhancers defines cellular subsets most associated to IBD and highlights the critical role of epigenetics in IBD. We review the central role of the interleukin 23 (IL-23) pathway in cellular plasticity, mechanisms which are significantly mediated by epigenetic regulation of master transcription factors of various CD4+ T-cell subsets. Present studies need to be complemented by a deeper understanding of intestine-specific gene expression and epigenetics, especially in mononuclear phagocytes, given their enormous plasticity, and tissue-dependent function. A deeper understanding and application of epigenetics may impact and guide early treatment and ultimately, disease prevention in IBD.

scholarly journals The Potential Role of Th9 Cell Related Cytokine and Transcription Factors in Patients with Hepatic Alveolar Echinococcosis

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Tuerhongjiang Tuxun ◽  
Shadike Apaer ◽  
Hai-Zhang Ma ◽  
Heng Zhang ◽  
Amina Aierken ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Potential Role ◽  
Alveolar Echinococcosis ◽  
Critical Role ◽  
Parasitic Infection ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mrna Levels ◽  
Human Host ◽  
Th9 Cells

Human alveolar echinococcosis (AE) is a lethal parasitic infectious disease which may lead to liver failure if left untreated. It is caused by the larval stage of the fox tapewormEchinococcus multilocularisand usually develops a substantial infiltrative occupation in solid organs. During the infection, T helper subsets are known to play crucial role in crosstalk between the parasite and human host. Th9 cells, a new member of CD4+T cell family which is characterized by its specific cytokine IL-9 and transcription factors PU.1 and IRF-4, have been known recently to have a critical role in allergic diseases, and cancers as well as the parasitic infection. To assess the potential role of Th9 cells during the infection, the mRNA levels of IL-9, PU.1, and IRF-4 both in peripheral blood mononuclear cells and in liver tissues were, respectively, detected by using real-time PCR. The plasma concentration levels of IL-9 were detected by using enzyme linked immunosorbent assay (ELISA). Th9 related cytokine IL-9 and transcription factors PU.1 and IRF-4 mRNA levels elevated both in PBMCs, and in hepatic lesion and paralesion tissues in AE patients. This may facilitate the infiltrative growth of the parasite and its persistence in human host.

scholarly journals The repression of nuclear factor I/CCAAT transcription factor (NFI/CTF) transactivating domain by oxidative stress is mediated by a critical cysteine (Cys-427)

2000 ◽  
Vol 348 (1) ◽  
pp. 235-240 ◽  
Author(s):  
Yannick MOREL ◽  
Robert BAROUKI
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Critical Role ◽  
Point Mutations ◽  
Dependent Manner ◽  
Nuclear Factor ◽  
Factor I ◽  
Nuclear Factor I

The activity of the nuclear factor I/CCAAT transcription factor (NFI/CTF) is negatively regulated by oxidative stress. The addition of relatively high (millimolar) H2O2 concentrations inactivates cellular NFI DNA-binding activity whereas lower concentrations can repress NFI/CTF transactivating function. We have investigated the mechanism of this regulation using Gal4 fusion proteins and transfection assays. We show that micromolar H2O2 concentrations repress the transactivating domain of NFI/CTF in a dose-dependent manner and are less or not active on other transcription factors' transactivating domains. Studies using deletions and point mutations pointed to the critical role of Cys-427. Indeed, when this cysteine is mutated into a serine, the repression by H2O2 is totally blunted. Mutation of other cysteine, serine and tyrosine residues within the transactivating domain had no clear effect on the repression by H2O2. Finally, treatment of cells with the thiol-alkylating reagent N-ethylmaleimide leads to a decrease in the transactivating function, which is dependent on Cys-427. This study shows that transactivating domains of transcription factors can constitute very sensitive targets of oxidative stress and highlights the critical role of these domains.

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