Sentences with phrase «activates other transcription factors»

Previous research found that Short - root activates other transcription factors as well, creating a cascade in which each gene - regulating protein controls the next in the root development pathway.

Not exact matches

The guilty protein is beta - catenin, a transcription factor which activates other genes.

The genes — Oct 3/4, Sox2, c - Myc and Klf4 — are molecular switches called transcription factors, which activate other genes in series like a power strip.

Glk1 is a transcription factor, meaning it binds to specific regions of DNA and activates genes involved in cell death and other plant immune responses.

FosB is a transcription factor in the brain which, together with other molecules, is involved in so - called signal transduction (transmission of stimuli to the cells), that is to say conveys genetic information between the cells and also determines whether certain genes are activated or not.

NF - κB is transcription factor that, among other functions, turns on genes involved in inflammation and immune response, and can be activated in the presence of pro-inflammatory cytokines.

Activated ERK1 / 2 modulates the functions of several transcription factors, protein kinases, protein phosphatases, cytoskeletal proteins, signaling molecules, apoptosis - related proteins, as well as other types of proteins [32], while activated AKT modulates the function of numerous substrates involved in the regulation of cell survival, cell cycle progression and cellular growth [33, 34], whereas JNK acts as pro-apoptotic as well as anti-apoptotic depending on the conditiActivated ERK1 / 2 modulates the functions of several transcription factors, protein kinases, protein phosphatases, cytoskeletal proteins, signaling molecules, apoptosis - related proteins, as well as other types of proteins [32], while activated AKT modulates the function of numerous substrates involved in the regulation of cell survival, cell cycle progression and cellular growth [33, 34], whereas JNK acts as pro-apoptotic as well as anti-apoptotic depending on the conditiactivated AKT modulates the function of numerous substrates involved in the regulation of cell survival, cell cycle progression and cellular growth [33, 34], whereas JNK acts as pro-apoptotic as well as anti-apoptotic depending on the conditions [35].

In the current study, the researchers found that EBNA2 and its related transcription factors activate some of the human genes associated with the risk for lupus and several other autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, inflammatory bowel disease, type 1 diabetes, juvenile idiopathic arthritis and celiac disease.

Among other actions, cells activate and then deactivate some types of transcription factors — proteins that...

This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma cell lines by modulating cell cycle arrest and apoptosis.26, 27 As a mechanism of action, KMT2D mutations of B - lymphoma cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or B - cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T - cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis of multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the differentiation and / or viability of PTCL - NOS through a PU.1 - dependent gene expression program.

In 2005, the identification of an activating mutation in JAK2 (the V617F mutation) as a STAT5 - activating and disease - causing genetic alteration in a significant proportion of patients with myeloproliferative neoplasms (MPNs) has emphasized the oncogenic role of the JAK tyrosine kinases in hematologic malignancies.2 — 5 JAK2 is a member of the Janus tyrosine kinase family comprising three other mammalian non-receptor tyrosine kinases (JAK1, JAK3 and TYK2) that associate with cytokine receptors lacking intrinsic kinase activity to mediate cytokine - induced signal transduction and activation of STAT transcription factors.6 All JAKs share a similar protein structure and contain a tyrosine kinase domain at the C - terminus flanked by a catalytically inactive pseudokinase domain with kinase - regulatory activity, by an atypical SH2 domain and by a FERM domain that mediates association to the membrane - proximal region of the cytokine receptors.7, 8 Soon after the discovery of JAK2 V617F, we and others described that activating JAK1 mutations are relatively common in adult patients with T - cell acute lymphoblastic leukemia (ALL) and participate in ALL development allowing for constitutive activation of STAT5.9 — 11 Several STAT5 - activating JAK1 mutations were also reported in AML and breast cancer patients.10

Under hypoxic conditions activates the transcription of over 40 genes, including, erythropoietin, glucose transporters, glycolytic enzymes, vascular endothelial growth factor, and other genes whose protein products increase oxygen delivery or facilitate metabolic adaptation to hypoxia.