Scientists uncover function of potential cancer-causing gene product

Aug 09, 2009

The Stowers Institute's Conaway Lab has uncovered a previously unknown function of a gene product called Amplified in Liver Cancer 1 (Alc1), which may play a role in the onset of cancer. The work was published yesterday by the Proceedings of the National Academy of Science Early Edition.

"We've been able to demonstrate that the protein encoded by the Alc1 gene is, in fact, a chromatin remodeling enzyme," explained Aaron Gottschalk, lead author on the paper and a University of Kansas Medical Center graduate student conducting research in the Conaway Lab. "By itself, this enzyme is inactive, but in the presence of a compound called NAD and another enzyme called poly (ADP-ribose) polymerase 1 (Parp1), its ability to move nucleosomes on DNA is strongly activated."

Parp1 uses NAD to build a polymeric molecule, poly(ADP-ribose), that is coupled to Parp1 itself or to other proteins. The team established that binding of a specific Alc1 region to poly(ADP-ribose) coupled to Parp1 helps recruit Alc1 to bind to and remodel nucleosomes.

"This finding is particularly interesting because Parp1 and poly(ADP-ribose) are known to play important roles in transcriptional regulation, , and , but how they do so is really not at all clear," said Ron Conaway, Ph.D., Investigator and co-senior author on the publication. "Finding that Parp1 and poly(ADP-ribose) recruit the chromatin remodeling Alc1 to and activate Alc1 activity suggests a mechanism by which they might function."

Medical researchers at universities and pharmaceutical companies are investigating Parp inhibitors for treatment of and other diseases. The team has shown that Parp inhibitors block Alc1 activities in the test tube and cells, suggesting that the therapeutic activities of these inhibitors could be due in part to indirect affects on Alc1. If true, drugs that target Alc1 function could also be useful in the treatment of disease.

Source: Stowers Institute for Medical Research

Explore further: New compounds protect nervous system from the structural damage of MS

add to favorites email to friend print save as pdf

Related Stories

Chromatin remodeling complex connected to DNA damage control

Aug 09, 2007

When molecular disaster strikes, causing structural damage to DNA, players in two important pathways talk to each other to help contain the wreckage, scientists at The University of Texas M. D. Anderson Cancer Center report ...

New therapies to treat breast, lymph cancer: studies

Jun 01, 2009

New therapies developed following groundbreaking clinical trials appear to effectively target breast cancer and non-Hodgkin's lymphoma, according to research unveiled Sunday at a major cancer conference.

Recommended for you

Mystery of the reverse-wired eyeball solved

Feb 27, 2015

From a practical standpoint, the wiring of the human eye - a product of our evolutionary baggage - doesn't make a lot of sense. In vertebrates, photoreceptors are located behind the neurons in the back of the eye - resulting ...

Neurons controlling appetite made from skin cells

Feb 27, 2015

Researchers have for the first time successfully converted adult human skin cells into neurons of the type that regulate appetite, providing a patient-specific model for studying the neurophysiology of weight ...

Quality control for adult stem cell treatment

Feb 27, 2015

A team of European researchers has devised a strategy to ensure that adult epidermal stem cells are safe before they are used as treatments for patients. The approach involves a clonal strategy where stem cells are collected ...

User comments : 1

Adjust slider to filter visible comments by rank

Display comments: newest first

E_L_Earnhardt
not rated yet Aug 10, 2009
The "gene" is only an entity of
electronic expression! COOLING drains
off the energy and slows mitosis!

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.