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10

The NF-κB family of transcription factors is very modular, with different combinations having different effects. The active (nuclear, DNA-bound) TF is a dimer, composed variously of RelA/p65, RelB, c-rel, NFKB1/p50, and/or NFKB2/p52 subunits. For example, the "canonical" p65/p50 dimer is activated in response to stimulants like TNF-α (tumor necrosis factor ...


10

You can validate the interactions by knockding down (KD) or overexpressing (OE) a gene and checking the change in expression levels of the downstream nodes. You can do this in a high throughput fashion using microarray or RNAseq. For protein you can do an LC-MS. However this method cannot help you in: Differentiating direct vs indirect interactions Finding ...


9

Here I will assume we are talking about eukaryotic sequence specific transcription factors (ssTFs) and try to answer your first and part of the second question. There is in any case not definitive answer yet. An estimate of ssTFs genes in humans is given in the 2009 Nature Reviews Genetics paper by Vaquerizas, JM et al, A census of human transcription ...


9

For a free resource, try GenMAPP. Commercial products like Ingenuity Pathway Analysis do the same thing with prettier graphics and a curated approach to network-building, but access can be expensive if you're not affiliated with an institution that will foot the bill.


9

Okay, I'll take this out of the comments and put in an answer for all of us to work on. To directly answer your question: "Is there an estimate for the percentage of these genes whose primary function is related to regulation of gene expression?" It depends on how you define "gene expression." And what cellular processes you want to include in ...


7

Yes, look at FANTOM and their work. There are about 2000 transcription factors and co-factors in the human genome. These are proteins, of course. If you add a couple (or few?) thousand microRNAs and a few dozen anti-sense transcripts, although small in size, you inch that percentage upwards. With some 70% of the human genome transcribed, by some estimates, ...


6

If you can't afford ingenuity, KEGG has branched out into regulatory networks as well. Here's the link to their version of the pathway. http://www.genome.jp/kegg/pathway/hsa/hsa04115.html Its free to use as a reference and for academic research.


5

Here are some examples: electric oscillators: neural activity cardiac automatism (0.8 ... 1 Hz) mechanical oscillators (as a result of neural activity): heart beats breathing (0.2 ... 0.3 Hz) intestinal peristaltic waves vocal chords activity (up to a few kHz) muscular spasm (pathological) chemical oscillators: insulin variation in concordance with ...


4

As you no doubt know, the term operator was coined by Jacob and Monod as part of the formalism they developed to explain the properties of certain mutants in the lac operon in E. coli. In physical terms it is indeed the site of binding of a transcription factor, the lac repressor. My understanding is that technically it is best to restrict the use of this ...


4

Here are 3: 1) gene knockout. Just delete the gene from the genome. The function is gone - useful for demonstrating a direct involvement of the gene in the phenotype. As a phenotype, the microarray will register all sorts of reactions to the loss of the gene in addition to the RNA in question being gone. 2) use selection to find mutants for the gene. ...


3

Positive co-operativity without feedback from the downstream genes: I guess Polycomb/Trithorax complexes will fit this criterion nicely. Polycomb group (PcG) represses Hox and other differentiation related genes (such as neurogenin) while Trithorax (TrxG) group promotes their expression. They are not like usual transcription factors that bind to promoters ...


3

So what you need is basically your data expressed as counts instead of proportions. Even if you do not have the matrix of counts as raw data, these proportions only needs to be multiplied by the total number of binding sites used in the study (e.g. the number of sequences that have been analysed) to get the counts (since proportion = count/total number of ...


3

This probably isn't the complete answer as I don't know so much about eukaryotic transcription, but maybe I can start the answer. First of all DNA bending can be sequence dependent - the double helix is not intrinsically straight. DNA is also pretty easy to bend - it spends most of its time coiled pretty easily around histones, and eukaryotes, supercoiled ...


3

Inferring transcriptional / regulatory networks from empirical data is an active area of research, and to my knowledge there aren't many mature tools for this type of analysis. I see mostly mathematicians, statisticians, and engineers working on this problem, probably because of the intense quantitative theory involved. Even if mature tools do exist, I doubt ...


3

If you have control expression values $c$ and e.g. disease expression values $d$, you take the ratio: $\frac{d}{c}$. If this is greater than one, it's up-regulated. Usually, the log-ratio is computed: $log\frac{d}{c}$. Now, if this is positive, the gene is up-regulated. Gene expression values are usually measured genome-wide and then normalized before ...


3

There was a paper published in Cell last year that has shown that the binding motif of a Hox transcription factor will change depending on whether there's a co-factor bound to the Hox. link to paper


2

Is there any relationship between DNA methylation as a level of stability to epigenetic states and genome size? I would say yes, because methylation is used to disable genes in differentiated cells. Disabled genes in differentiated cells generally need to stay disabled to maintain normal behavior for the cell type. Larger genomes usually encode more ...


2

Removal of 5' cap is essential for degradation by 5'→3' exonucleases such as Xrn1/2. Xrn1/2 is constitutive and degradation of uncapped RNAs would be quite fast (don't have a reference for the exact lifetime). Deadenylation generally precedes 3'→5' degradation by exosome but I am not sure if that is a prerequisite. However tailless mRNAs can be stabilized by ...


2

Heterochromatin profile is of course different in different cells but I am not sure if absolute heterochromatin content will vary greatly. This DNAse hypersensitivity region data is for human cells but same principles apply to all organisms. If I have to take a guess then I would say that quiescent cells are likely to have more heterochromatin. ...


2

There's no rule that says a transcription factor must be either a repressor or an activator. The lambda repressor (CI) is in fact a repressor and activator of transcription, depending on where it is bound and to what promoter you are referring to. I know your question isn't directly about lambda phage, but I think this mechanism may be best explained in the ...


2

I'm tempted to say, "It's complicated." CI does indeed act as both a repressor and activator. Transcription regulation in the lambda bacteriophage is quite complex for such a small system, so some confusion is understandable. Lewis et al. gives a rough description in a relatively recent paper (1): The CI protein autoregulates its synthesis. At low ...


2

Since @biogirl has given an answer, I'll add my opinion: β-galactosidase would be expressed but the permease and transacetylase would not. The operator lies adjacent to/slightly overlaps the promoter, upstream of the lacZ gene. Binding of the repressor to the operator blocks the promoter, and induction of theoperon involves the repressor leaving the ...


2

Interesting question. I think I have two examples for you which might be interesting. The first is the co-regulation of the microphthalmia-associated transcription factor (MITF) in pigmentation by SOX10 and PGC1a/b. See this paper: PGC-1 coactivators regulate MITF and the tanning response. The second is about the regulation of brown fat tissue by PGC1a ...


1

Generally speaking, heterochromatin or euchromatin structures mark specific regions to regulate the transcriptional activity and these marks carry the signature of developmental processes as they differ in different tissues (or cell types). Therefore, we should not ignore the developmental processes if we want to understand how such epigenetic marks are ...


1

I believe the answer should be that permease is expressed. As you can see from the image, if the operator is moved between Z gene and Y gene, Y gene should be expressed and permease should be made.


1

Dicer is an endo-ribonuclease belonging to the RNAse-III class. Dicer is not a part of the RISC. It however helps in the formation of RISC by cleaving dsRNA or the stem of hairpin RNA on two ends which liberates a small dsRNA product. Then one of the strands is loaded into the RISC. There are several reviews on this topic and there is a video as well which ...


1

There are no reports for it yet. I don't think just because they show overall homology, they would exhibit crosstalk. Just see the alignment of the DNA binding domains of these proteins first ~70 residues from N-terminal. Moreover their DBDs belong to different PFAM families. Similarly with the promoter sequences. As reported in iGEM website: Mnt ...


1

As Alan Boyd said, this process is called trans splicing where exons of different RNAs are joined together. Physical proximity is conducive for trans-splicing. This study shows that trans-splicing frequency is higher if the genes are proximal. Proximity not only means closer in the genome but also the 3D proximity governed by chromosomal interactions. Now, ...


1

I'd like to add regulonDB which is not as integrated, but has a tremendous map of the e coli regulome which would be useful for any bacterial model. I agree with @DanielStandage that this is not a well understood and there don't even appear to be standard representations for this sort of data.



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