Showing posts with label stressors. Show all posts
Showing posts with label stressors. Show all posts

Thursday, March 21, 2013

IXL Gene in pancreatic cancer

IXL, Intersex like cell, a survival regulator, located on 19q13,
note the q location of the amplicon ( a piece of DNA or RNA that is the source and/or product of natural or artificial amplification or replication events) the 10% rate of amplification is clearly higher than the usual few, with 5% of secondary amplification making this a clear Amplicon.  Knocking down this stops cells in Go-G1 per Kuuselo et al.  As the Component of the Mediator complex, it is a co-activator that  regulates the transcription of nearly all RNA polymerase II-dependent genes which are at the origin of m-RNA formation.  It puts this gene at the initiation complex.  At the sole of enzyme fabrication, regulator fabrication, and formation of transcription factors.  Tinkering with gene blocks transcription. That's it!  Even splicing will in fact be affected to some extent.

This gene interacts with AP-1

and

AP-1 transcription factor

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AP-1/DNA complex. Crystallographic structure (PDB 1FOS) of the AP-1 heterodimer comprising c-Fos (cyan) and c-Jun (green) complexed with DNA (brown).
In the field of molecular biology, the activator protein 1 (AP-1) is a transcription factor which is a heterodimeric protein composed of proteins belonging to the c-Fos, c-Jun, ATF and JDP families. It regulates gene expression in response to a variety of stimuli, including cytokines, growth factors, stress, and bacterial and viral infections.[1] AP-1 in turn controls a number of cellular processes including differentiation, proliferation, and apoptosis.[2]
AP-1 upregulates transcription of genes containing the TPA DNA response element (TRE; 5'-TGAG/CTCA-3').[1] AP-1 binds to this DNA sequence via a basic amino acid region, while the dimeric structure is formed by a leucine zipper.[3] 

SO HERE PANCREATITIS, ALCOHOL, VIRUSES AND OTHER STRESSORS FIND THEIR WAY TO THE PATHOGENESIS OF PANCREATIC CANCERS!

It is also connected to

CUTL1

and it needs CUTL-1 now to have muscle, but unleash the powerful regulator it encloses.  It may use this regulator to silence other genes that may lead to apoptosis. The IXL gene is a strategist in its advancement of pancreatic cancer.  This is a major target!

And 3rd, and not the least 

it interferes with ATF2

'This gene encodes a transcription factor that is a member of the leucine zipper family of DNA-binding proteins. This protein binds to the cAMP-responsive element (CRE), an octameric palindrome. The protein forms a homodimer or heterodimer with c-Jun and stimulates CRE-dependent transcription. The protein is also a histone acetyltransferase (HAT) that specifically acetylates histones H2B and H4 in vitro; thus, it may represent a class of sequence-specific factors that activate transcription by direct effects on chromatin components. Additional transcript variants have been identified but their biological validity has not been determined.[1]
The gene atf2 is located at human chromosome 2q32.[2] '  (wikipedia

BELIEVE ME WHEN THEY SAY LEUCINE, THE MTORs ARE NOT FAR BEHIND!!!