SOME LITTLE GENES WITH A BIG IDEA: SHP GENE

IF YOU KNOW HOW IMPORTANT ESTROGEN RECEPTORS ARE IN BREAST CANCERS,
IF YOU KNOW HOW IMPORTANT ANDROGEN RECEPTORS ARE IN PROSTATE CANCER
IF YOU REALIZE HOW IMPORTANT THE THYROID FUNCTION IS DRIVING THE RATE OF METABOLISM
IF YOU REALIZE THE DIFFICULTY THAT POSES HEPATOMA IN TERMS OF TREATMENT,
IF YOU KNOW THAT SARCOMA IS TOUGH TO TREAT,

THEN YOU SHOULD DIG DEEPER IN UNDERSTANDING THAT ALL THESE RECEPTORS HAVE ONLY ONE INHIBITOR, THE "SMALL HETERODIMER PARTNER"  GENE!

WHAT IS IT AND HOW AND WHEN SHOULD IT COME IN?

Small heterodimer partner has been shown to interact with:

• Androgen receptor,^[4]
• Estrogen receptor alpha,^[5]
• Hepatocyte nuclear factor 4 alpha,^[6]
• Liver receptor homolog-1,^[7][8]
• Liver X receptor alpha,^[7]
• Peroxisome proliferator-activated receptor gamma,^[9]
• Retinoic acid receptor alpha,^[10][11] and
• Retinoid X receptor alpha.^[6][7]

I refuse to comment on the PPARgamma for now, did you know that this is the staff that interacts with Rb1?  watch it as it is coming to a Diabetic control and evaluation near you!

At CRBCM we are working hard!

KNOW THIS: A little bit of good news in the nation !

"Diabetes report card chronicling how the United States is faring in terms of management of the condition in adults, based on data to 2010, shows that there has been improvement, but there are still large gaps in terms of the control of 2 important risk factors, smoking and hypertension." (Medscape)".

NOMENCLATURE OF GENES AND PATHWAYS INVOLVED IN BUTEIN INHIBITIONS: IKK and Sirtuin

IKK:
The subunit to be inhibited for the activation of the Nuclear factor and pathway NF-kB which has versatile transforming capacity to combat, escape and resist various attackers including infection and chemotherapy.  Inhibition here reduces the cell capacity to adapt.  It appears that the Transcription factor NFkB is sitting there in the Cytosol totally inactive, touch the IKK through phosphorylation, wakes the NFkB which spring into motion and unleashes its power.  One of the best described pathway flow is TNF posphorylation of IKK which detaches and goes on to  being ubiquitinated and degraded through the Proteasome.  detachment of the IKK lead to a free NFkB kinase which enter the nucleus to unleash all kinds of genes of defense.  DO REMEMBER that upstream NFkB go through MEK (also involved in Angiogenesis) to reach MAP3K and you can see how through networking of these pathways the phenomena gets global.

Sirtuin:
This compound is SIRT1, it is  activated by BUTEIN
Butein actually activate SIRT1 and may induce aging in the cell.  Remember Butein by activating Sirtuin will have a role in Diabetes, Gout, Alzheimer dementia, and Amyloid related disease.  Butein, a versatile anti-inflammatory drug with effect on NAD (Nicotinamid), and may be a Histone De-acetylase inhibitor. This stuff has potential! 

NON-CASPASE WAY TO CELL DEATH
ONE OF THE WAYS CELLS DIE WHICH IS NON-CASPASE DRIVEN MAY RESULT FROM DISRUPTION TO THE CONCENTRATION OF THE CYTOSOL OR SOLUTION WITHIN THE CELL.   HOMEOSTASIS REQUIRES THAT SOLUTION TO BE SET AT A CERTAIN CONCENTRATION IN TERMS OF ELECTROLYTES, OXYGEN AND PH.  THE CELL HAS ION PUMPS TO MAINTAIN ELECTROLYTE CONCENTRATION.  ELECTIVE DISRUPTION OF ION PUMPS WILL LEAD TO DISRUPTION OF CONCENTRATIONS THAT MAY SEND DEVASTATING BLOW TO THE CELL.   WATER GOES FROM LESS CONCENTRATED TO MORE CONCENTRATED ENVIRONMENTS.  THIS IS A POWERFUL KNOWN LAW OF NATURE.  IN CLINICAL PRACTICE, WE DON'T USE THIS LAW ENOUGH.  NOT BECAUSE IT IS NOT REAL
BECAUSE THIS IS HOW DIABETES KILLS ITS VICTIMS.  THIS IS HOW DEHYDRATION KILLS AND SO ON.   OUR CHALLENGE HAS BEEN HOW TO ELECTIVELY USE IT TO ATTACK ONLY CANCER CELLS.  FOR THIS WE NEED TO FIND OUT IF IONS PUMPS FROM CANCER CELLS ARE DIFFERENT FROM THOSE OF NORMAL CELLS.

(TO BE CONTINUED)