Showing posts with label PTK2. Show all posts
Showing posts with label PTK2. Show all posts

Wednesday, October 30, 2013

Genetic basis of Autism

The notion that an inflammatory process such as the one induced by an immunization may contribute to children's mental retardation or Autism has fundamental truth when it comes to gene pathways. Indeed, during an acute inflammatory insult, Macrophages that are called to the theater will liberate several cytokines which include TGF alpha.  This cytokine will bind to EGFR receptors while other cytokines induced by the inflammatory process will bind their relevant receptors.  Internalization of these receptors will leave deep edges at the membrane, activating the Focal adhesion molecules of Kinase (FAK ).  The first known gene to react with the FAK gene is the Tuberous sclerosis gene which is known to lead to Autism.  In a forming or developing brain, certain isoforms of this gene may predispose some children to develop autism.   The crux of the problem is to determine which inflammatory process (immunization or other processes) is at the source of the problem!

PTK2 protein tyrosine kinase 2 (PTK2), also known as Focal Adhesion Kinase (FAK), is a protein that, in humans, is encoded by the PTK2 gene.[2] PTK2 is a focal adhesion-associated protein kinase involved in cellular adhesion (how cells stick to each other and their surroundings) and spreading processes (how cells move around).[3] It has been shown that when FAK was blocked, breast cancer cells became less metastatic due to decreased mobility.[4]

 PTK2 has been shown to interact with TSC2, (22 wikipedia)

 Tuberin also known as tuberous sclerosis 2 is a protein that in humans is encoded by the TSC2 gene.
 About 50% of people with TSC have learning difficulties ranging from mild to significant,[2] and studies have reported that between 25% and 61% of affected individuals meet the diagnostic criteria for autism, with an even higher proportion showing features of a broader pervasive developmental disorder.[3] A 2008 study reported self-injurious behavior in 10% of people with TSC.[4] Other conditions, such as ADHD, aggression, behavioral outbursts and OCD (obsessive compulsive disorder) can also occur. Lower IQ is associated with more brain involvement on MRI.(wikipedia)


Tuesday, February 5, 2013


As we speak with the University of Texas in El Paso, the CRBCM would like to look further into the clinical use of a potent Inhibitor in a phase I study.  We believe this compound will have a significant role in Triple Negative Breast Cancer.  Butein, a derivative of Charcone, a powerful anti-Oxidant and known anti-inflammatory used in ASIA, seems to have a global inhibitory effect.  It is one of the 3 inhibitors of the SRC, it is a Glutathione inhibitor, Blocker of EGF, inhibitor of IKK, and of the NF-kB signal transduction pathway, cause phosphorylation of the AKT, reduction of Cyclin D1 and D2,  activation of WAF1/p21 and KIP1/p27, Iron induced inhibitor of Xanthine Oxidase (love that enzyme since I first learned about Asthma).
This Butein stuff is a global inhibitor.  If you add this to MTOR inhibitors, you may end up with too toxic a combination for any cancer! This would be an overwhelming attack on cells!

It has demonstrated powerful Ex-vivo activity against breast and prostate cancer cell lines, and is empirically used against Gastric cancer.

This global and versatile inhibitor, Butein, should have activity in Sarcoma since it inhibits SRC and potentially the fibroblast.  Other Inhibitors of SRC, heme supported phosphorylation and CYIKYYF.  (of note CDK1, PTRC and PTK2)
Gave you so many letters, lets move to gene Nomenclature please!  we are still working hard at the CRBCM!