Sentences with phrase «for other transcription factors»

They may exert a transcriptional function or act as comodulators for other transcription factors.

Not exact matches

«But in this case, when this virus infects cells, the virus makes its own transcription factors, and those sit on the human genome at lupus risk variants (and at the variants for other diseases) and that's what we suspect is increasing risk for the disease.»

The activity of four transcription factors — proteins that regulate the expression of other genes — appears to distinguish the small proportion of glioblastoma cells responsible for the aggressiveness and treatment resistance of the deadly brain tumor.

Affected family members, the group found, had inherited one or two defective copies of ZIC3, a previously unknown gene that appears to code for a transcription factor — a protein that switches other genes on or off.

Transcription - factor genes code for proteins that regulate the activity of other genes and so affect an animal's ability to respond to its environment.

In most cases, the genes responsible for these processes are known as «transcription factors» — meaning that they are responsible for turning other genes on and off.

All of these genes code for transcription factors, which are proteins that control the expression of other genes.

«Interestingly, because deltaFosB is a transcription factor, meaning that its job is to regulate the expression of other proteins, these findings led us to predict that the increased deltaFosB levels might be responsible for suppressing the production of proteins that are necessary for learning and memory,» Chin said.

As for next research steps, the investigators will seek to exploit the SRY database and its evolutionary linkages to other SOX transcription factors to explore applications to stem - cell biology and cancer.

She likens TCF - 1 to an icebreaker ship that initially opens the ice (condensed, closed chromatin) and keeps a path available for other ships (other transcription factors that work in later stages of development) to steam through the now - open water (unwound chromatin).

Now, a collaboration between the RIKEN Center for Integrative Medical Science (IMS) and other institutions in Japan and Europe have found that in immune cells, simply blocking a transcription factor that leads to differentiation is sufficient to keep cells in a multipotent stem cell - like state where they can continue to proliferate and can later differentiate into various cell types.

The variant allele disrupts predicted binding sites for two transcription factors (MEF2C and CDX2) and creates possible binding sites for at least two others.

So what we think is that probably in many cells in this section, all cells, the chromatin is encountered in a specific state, and in order to render the cell is permissive to reprogramming, you have to overcome these certain epigenetic modifications that block, for example, the binding of Ascl1 to its target chains, or the binding of other transcription factors to its target chains, then this way interfere with the possibility of reprogramming.

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.

Using novel gene - array technology to measure the extent of gene expression in thousands of genes simultaneously, this study shows that as humans diverged from their ape ancestors in the last five million years, genes for transcription factors — which control the expression of other genes — were four times as likely to have changed their own expression patterns as the genes they regulate.

Other projects focus on studying how mutations found in the genes for skeletogenic transcription factors cause skeletal and other defects in human patients and finding ways to overcome the negative effects of these mutations in patiOther projects focus on studying how mutations found in the genes for skeletogenic transcription factors cause skeletal and other defects in human patients and finding ways to overcome the negative effects of these mutations in patiother defects in human patients and finding ways to overcome the negative effects of these mutations in patients.

«Not only are these transcription factors vital for turning on certain genes, but their interaction is important to keep each other from going to the wrong place and turning on a set of genes that doesn't belong in a heart cell.»

TCF - 1 is like an icebreaker ship that initially opens the ice (condensed, closed chromatin) and keeps a path available for other ships (other transcription factors that work in later stages of development) to steam through the now - open water (unwound chromatin).

The other major transcription factor involved in IL - 22 production is the aryl hydrocarbon receptor (AHR), which is important not only for Il22 expression in ILC3s [28], but also for the development of ILC3s from immature precursors [29].

Besides, some other potential cis - acting elements for transcription factors [such as CAAT / enhancer binding protein (C / EBP) and PU.1] have been also noted in the RIG - G gene promoter.

By learning the rules for these three proteins, the scientists say they can infer the rules of other transcription factors that are also important for heart development.

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

STAT1 and STAT2 represent two of the seven mammalian STAT proteins that share several structurally and functionally conserved domains, including an NH2 - terminal coiled - coil region for interactions with other transcription factors and chaperone proteins, a phosphotyrosine - binding Src homology 2 domain required for receptor binding and STAT dimerization, and a COOH - terminal transcription activation domain (TAD) within which a highly conserved tyrosine residue is present.

As for myself, I will pick up articles in prebiotic chemistry, virology as it relates to retroviruses or bacterial viruses, or molecular biology, such as those dealing with new discoveries related to promoters, transcription factors (proteins and RNAs which regulate the expression of other proteins and RNAs by binding to promoters), but even after having read a fair amount, trying to fit together pieces in a puzzle, I will be lucky if I have actually understood more than half of a given article at a relatively basic level.