scholarly journals Estrogen-TGFβ cross-talk in bone and other cell types: Role of TIEG, Runx2, and other transcription factors

2008 ◽  
Vol 103 (2) ◽  
pp. 383-392 ◽  
Author(s):  
J. R. Hawse ◽  
M. Subramaniam ◽  
J. N. Ingle ◽  
M. J. Oursler ◽  
N. M. Rajamannan ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Cross Talk ◽  
Cell Types

The paracaspase MALT1 in psoriasis

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Stephan Hailfinger ◽  
Klaus Schulze-Osthoff
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Transcription Factors ◽  
Skin Disease ◽  
Cell Types ◽  
Cytokine Receptors ◽  
Molecular Scaffold ◽  
Therapeutic Implications ◽  
Stimulation Of

Abstract Psoriasis is a frequent autoimmune-related skin disease, which involves various cell types such as T cells, keratinocytes and dendritic cells. Genetic variations, such as mutations of CARD14, can promote the development of the disease. CARD14 mutations as well as the stimulation of immune and cytokine receptors activate the paracaspase MALT1, a potent activator of the transcription factors NF-κB and AP-1. The disease-promoting role of MALT1 for psoriasis is mediated by both its protease activity as well as its molecular scaffold function. Here, we review the importance of MALT1-mediated signaling and its therapeutic implications in psoriasis.

Regulation of Pax-3 expression in the dermomyotome and its role in muscle development

Development ◽  
1994 ◽  
Vol 120 (4) ◽  
pp. 957-971 ◽  
Author(s):  
M. Goulding ◽  
A. Lumsden ◽  
A.J. Paquette
Keyword(s):  
Transcription Factors ◽  
Muscle Development ◽  
Cell Types ◽  
Axial Skeleton ◽  
Mouse Embryos ◽  
Related Gene ◽  
Paired Domain ◽  
Trunk Musculature ◽  
Somitic Mesoderm

The segmented mesoderm in vertebrates gives rise to a variety of cell types in the embryo including the axial skeleton and muscle. A number of transcription factors containing a paired domain (Pax proteins) are expressed in the segmented mesoderm during embryogenesis. These include Pax-3 and a closely related gene, Pax-7, both of which are expressed in the segmental plate and in the dermomyotome. In this paper, we show that signals from the notochord pattern the expression of Pax-3, Pax-7 and Pax-9 in somites and the subsequent differentiation of cell types that arise from the somitic mesoderm. We directly assess the role of the Pax-3 gene in the differentiation of cell types derived from the dermomyotome by analyzing the development of muscle in splotch mouse embryos which lack a functional Pax-3 gene. A population of Pax-3-expressing cells derived from the dermomyotome that normally migrate into the limb are absent in homozygous splotch embryos and, as a result, limb muscles are lost. No abnormalities were detected in the trunk musculature of splotch embryos indicating that Pax-3 is necessary for the development of the limb but not trunk muscle.

scholarly journals Role of Forkhead Transcription Factors in Diabetes-Induced Oxidative Stress

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Bhaskar Ponugoti ◽  
Guangyu Dong ◽  
Dana T. Graves
Keyword(s):  
Oxidative Stress ◽  
Transcription Factors ◽  
Cellular Response ◽  
Cell Damage ◽  
Cell Types ◽  
Biological Processes ◽  
Oxygen Species ◽  
Forkhead Transcription Factors ◽  
Foxo Transcription Factors

Diabetes is a chronic metabolic disorder, characterized by hyperglycemia resulting from insulin deficiency and/or insulin resistance. Recent evidence suggests that high levels of reactive oxygen species (ROS) and subsequent oxidative stress are key contributors in the development of diabetic complications. The FOXO family of forkhead transcription factors including FOXO1, FOXO3, FOXO4, and FOXO6 play important roles in the regulation of many cellular and biological processes and are critical regulators of cellular oxidative stress response pathways. FOXO1 transcription factors can affect a number of different tissues including liver, retina, bone, and cell types ranging from hepatocytes to microvascular endothelial cells and pericytes to osteoblasts. They are induced by oxidative stress and contribute to ROS-induced cell damage and apoptosis. In this paper, we discuss the role of FOXO transcription factors in mediating oxidative stress-induced cellular response.

scholarly journals Proto-oncogenes of the fos/jun family of transcription factors are positive regulators of myeloid differentiation.

1993 ◽  
Vol 13 (2) ◽  
pp. 841-851 ◽  
Author(s):  
K A Lord ◽  
A Abdollahi ◽  
B Hoffman-Liebermann ◽  
D A Liebermann
Keyword(s):  
Transcription Factors ◽  
Leucine Zipper ◽  
Culture Media ◽  
Terminal Differentiation ◽  
Cell Types ◽  
Primary Response ◽  
Myeloid Differentiation ◽  
Active Transcription

The proto-oncogenes c-jun, junB, junD, and c-fos recently have been shown to encode for transcription factors with a leucine zipper that mediates dimerization to constitute active transcription factors; juns were shown to dimerize with each other and with c-fos, whereas fos was shown to dimerize only with juns. After birth, hematopoietic cells of the myeloid lineage, and some other terminally differentiated cell types, express high levels of c-fos. Still, the role of fos/jun transcription factors in normal myelopoiesis or in leukemogenesis has not been established. Recently, c-jun, junB, and junD were identified as myeloid differentiation primary response genes stably expressed following induction of terminal differentiation of myeloblastic leukemia M1 cells. Intriguingly, c-fos, though induced during normal myelopoiesis, was not induced upon M1 differentiation. To gain further insights into the role of fos/jun in normal myelopoiesis and leukemogenicity, M1fos and M1junB cell lines, which constitutively express c-fos and junB, respectively, were established. It was shown that enforced expression of c-fos, and to a lesser extent junB, in M1 cells results in both an increased propensity to differentiate and a reduction in the aggressiveness of the M1 leukemic phenotype. M1fos cells constitutively expressed immediate-early and late genetic markers of differentiated M1 cells. The in vitro differentiation of normal myeloblasts into mature macrophages and granulocytes, as well as the increased propensity of M1fos leukemic myeloblasts to be induced for terminal differentiation, was dramatically impaired with use of c-fos antisense oligomers in the culture media. Taken together, these observations show that the proto-oncogenes which encode for fos/jun transcription factors play important roles in promoting myeloid differentiation. The ability of the M1 leukemic myeloblasts to be induced for terminal differentiation in the absence of apparent fos expression indicates that there is some redundancy among the fos/jun family of transcription factors in promoting myeloid differentiation; however, juns alone cannot completely compensate for the lack of fos. Thus, genetic lesions affecting fos/jun expression may play a role in the development of "preleukemic" myelodysplastic syndromes and their further progression to leukemias.

scholarly journals Corticosteroid receptors, macrophages and cardiovascular disease

2009 ◽  
Vol 42 (6) ◽  
pp. 449-459 ◽  
Author(s):  
Amanda J Rickard ◽  
Morag J Young
Keyword(s):  
Cardiovascular Disease ◽  
Transcription Factors ◽  
Glucocorticoid Receptor ◽  
Mineralocorticoid Receptor ◽  
Cell Types ◽  
Current Understanding ◽  
Corticosteroid Receptors ◽  
Monocytes And Macrophages ◽  
Anti Inflammatory

The mineralocorticoid receptor (MR) and glucocorticoid receptor are ligand-activated transcription factors that have important physiological and pathophysiological actions in a broad range of cell types including monocytes and macrophages. While the glucocorticoids cortisol and corticosterone have well-described anti-inflammatory actions on both recruited and tissue resident macrophages, a role for the mineralocorticoid aldosterone in these cells is largely undefined. Emerging evidence, however, suggests that MR signalling may promote pro-inflammatory effects. This review will discuss the current understanding of the role of corticosteroid receptors in macrophages and their effect on diseases involving inflammation, with a particular focus on cardiovascular disease.

scholarly journals FOXO Transcription Factors: Their Clinical Significance and Regulation

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Yu Wang ◽  
Yanmin Zhou ◽  
Dana T. Graves
Keyword(s):  
Transcription Factors ◽  
Cellular Proliferation ◽  
Cell Types ◽  
Mitogen Activated Protein Kinase ◽  
Survival Pathways ◽  
Mitogen Activated Protein ◽  
Foxo Transcription Factors ◽  
Phosphoinositide 3 Kinase ◽  
Clinical Conditions

Members of the class O of forkhead box transcription factors (FOXO) have important roles in metabolism, cellular proliferation, stress resistance, and apoptosis. The activity of FOXOs is tightly regulated by posttranslational modification, including phosphorylation, acetylation, and ubiquitylation. Activation of cell survival pathways such as phosphoinositide-3-kinase/AKT/IKK or RAS/mitogen-activated protein kinase phosphorylates FOXOs at different sites which regulate FOXOs nuclear localization or degradation. FOXO transcription factors are upregulated in a number of cell types including hepatocytes, fibroblasts, osteoblasts, keratinocytes, endothelial cells, pericytes, and cardiac myocytes. They are involved in a number of pathologic and physiologic processes that include proliferation, apoptosis, autophagy, metabolism, inflammation, cytokine expression, immunity, differentiation, and resistance to oxidative stress. These processes impact a number of clinical conditions such as carcinogenesis, diabetes, diabetic complications, cardiovascular disease, host response, and wound healing. In this paper, we focus on the potential role of FOXOs in different disease models and the regulation of FOXOs by various stimuli.

Neuron-glia: understanding cellular copper homeostasis, its cross-talk and their contribution towards neurodegenerative diseases

Metallomics ◽  
2020 ◽  
Author(s):  
Ashima Bhattacharjee ◽  
Sandeepan Ghosh ◽  
Ajanta Chatterji ◽  
Kaustav Chakraborty
Keyword(s):  
Neurodegenerative Diseases ◽  
Cross Talk ◽  
Copper Homeostasis ◽  
Cell Types ◽  
Principal Cell ◽  
Cellular Copper

The review focuses on the role of the copper homeostasis in the principal cell types of the CNS and its role in neurodegenration.

scholarly journals Insight Cross-talk between p53 and Toll-like Receptor

2021 ◽  
pp. 23-29
Author(s):  
Mohammad Jahoor Alam ◽  
Fevzi Bardakci ◽  
Sadia Anjum ◽  
Shumayla Rasheed Mir ◽  
Irfan Ahmad ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Transcription Factors ◽  
Cross Talk ◽  
Experimental Studies ◽  
Therapeutic Interventions ◽  
Toll Like Receptor ◽  
Transcription Activator ◽  
Molecular Patterns ◽  
Broad Understanding

Toll-like receptors (TLR) are one of the most-studied receptors for their role in innate immunity. TLRs are reported to binds with conserved pathogen-associated molecular patterns (PAMPS). TLRs and PAMPS interaction leads to several downstream proteins' activation, which further signaled to the various transcription factors. Moreover, these transcription factors play an important role in synthesizing proteins that control cellular immunity. Various TLR proteins have been reported in humans as well several other organisms. Studies show that apart from inducing innate immunity, TLRs have also played an important role in the induction of many proteins, and protein networks associated with initiation apoptosis and cancer prevention. P53 is one of the most important and widely studied proteins. Moreover, various experimental studies suggest that p53 has an important role as tumor suppressor. It is reported that more than 50% of cancerous growth are associated with the mutation of p53. It acts as transcription activator for several proteins that are mostly associated with glycolysis, cell cycle, cell differentiation, apoptosis and cancer. In the present review, we present an insight cross-talk between p53 and Toll-like receptor. In addition, the well-characterized role of p53 in the regulation of the immune system is studied, which would provide a new insight to the broad understanding of p53 role in human biology. Moreover, the association of the p53 and TLRs can lead to therapeutic interventions.

scholarly journals The “Janus” Role of C/EBPs Family Members in Cancer Progression

2020 ◽  
Vol 21 (12) ◽  
pp. 4308 ◽  
Author(s):  
Manlio Tolomeo ◽  
Stefania Grimaudo
Keyword(s):  
Transcription Factors ◽  
Cancer Progression ◽  
Tumor Suppressors ◽  
Cellular Response ◽  
Cellular Proliferation ◽  
Cell Types ◽  
Tumor Promoters ◽  
Expression Of Genes ◽  
Molecular Aspects

CCAAT/enhancer-binding proteins (C/EBPs) constitute a family of transcription factors composed of six members that are critical for normal cellular differentiation in a variety of tissues. They promote the expression of genes through interaction with their promoters. Moreover, they have a key role in regulating cellular proliferation through interaction with cell cycle proteins. C/EBPs are considered to be tumor suppressor factors due to their ability to arrest cell growth (contributing to the terminal differentiation of several cell types) and for their role in cellular response to DNA damage, nutrient deprivation, hypoxia, and genotoxic agents. However, C/EBPs can elicit completely opposite effects on cell proliferation and cancer development and they have been described as both tumor promoters and tumor suppressors. This “Janus” role of C/EBPs depends on different factors, such as the type of tumor, the isoform/s expressed in cells, the type of dimerization (homo- or heterodimerization), the presence of inhibitory elements, and the ability to inhibit the expression of other tumor suppressors. In this review, we discuss the implication of the C/EBPs family in cancer, focusing on the molecular aspects that make these transcription factors tumor promoters or tumor suppressors.

scholarly journals Proto-oncogenes of the fos/jun family of transcription factors are positive regulators of myeloid differentiation

1993 ◽  
Vol 13 (2) ◽  
pp. 841-851
Author(s):  
K A Lord ◽  
A Abdollahi ◽  
B Hoffman-Liebermann ◽  
D A Liebermann
Keyword(s):  
Transcription Factors ◽  
Leucine Zipper ◽  
Culture Media ◽  
Terminal Differentiation ◽  
Cell Types ◽  
Primary Response ◽  
Myeloid Differentiation ◽  
Active Transcription

The proto-oncogenes c-jun, junB, junD, and c-fos recently have been shown to encode for transcription factors with a leucine zipper that mediates dimerization to constitute active transcription factors; juns were shown to dimerize with each other and with c-fos, whereas fos was shown to dimerize only with juns. After birth, hematopoietic cells of the myeloid lineage, and some other terminally differentiated cell types, express high levels of c-fos. Still, the role of fos/jun transcription factors in normal myelopoiesis or in leukemogenesis has not been established. Recently, c-jun, junB, and junD were identified as myeloid differentiation primary response genes stably expressed following induction of terminal differentiation of myeloblastic leukemia M1 cells. Intriguingly, c-fos, though induced during normal myelopoiesis, was not induced upon M1 differentiation. To gain further insights into the role of fos/jun in normal myelopoiesis and leukemogenicity, M1fos and M1junB cell lines, which constitutively express c-fos and junB, respectively, were established. It was shown that enforced expression of c-fos, and to a lesser extent junB, in M1 cells results in both an increased propensity to differentiate and a reduction in the aggressiveness of the M1 leukemic phenotype. M1fos cells constitutively expressed immediate-early and late genetic markers of differentiated M1 cells. The in vitro differentiation of normal myeloblasts into mature macrophages and granulocytes, as well as the increased propensity of M1fos leukemic myeloblasts to be induced for terminal differentiation, was dramatically impaired with use of c-fos antisense oligomers in the culture media. Taken together, these observations show that the proto-oncogenes which encode for fos/jun transcription factors play important roles in promoting myeloid differentiation. The ability of the M1 leukemic myeloblasts to be induced for terminal differentiation in the absence of apparent fos expression indicates that there is some redundancy among the fos/jun family of transcription factors in promoting myeloid differentiation; however, juns alone cannot completely compensate for the lack of fos. Thus, genetic lesions affecting fos/jun expression may play a role in the development of "preleukemic" myelodysplastic syndromes and their further progression to leukemias.

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