For the first time, findings by scientists at the Genome Institute of Singapore (GIS) may be paving the way for more efficient analyses and tests related to the replication of cells, and ultimately, to the better understanding of human biology, such as in stem cell research.

Faithful duplication of the genome (the hereditary information that is encoded in genetic materials known as DNA) ensures that daughter cells inherit a complete set of genetic materials identical to parent cells. This duplication occurs in the section of the cell cycle known as the S-phase. Extensive research on the budding yeast, an organism often used in modern cell biology research, had revealed that the replication process is initiated at hundreds of origins in the S-phase.

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Nerve cells must perform millions of neuronal processes and form connections between them during embryonic development to ensure that the nervous system will function properly. Dr. Marta Rosário and Prof. Walter Birchmeier from the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch (Germany), a member of the Helmholtz-Association of National Research Centres, have discovered a novel regulator which is crucial for this process and which they named NOMA-GAP (Neurite-Outgrowth MultiAdaptor RhoGAP).

They show that NOMA-GAP is essential for the function of the nerve growth factor (NGF), itself a crucial factor for the functioning of the nervous system and for nerve cell survival.

Mayo Clinic researchers have identified the first immune molecule that appears to play a role in prostate cancer development and in predicting cancer recurrence and progression after surgery. The report on the B7-H3 molecule by Mayo Clinic Cancer Center appears today in Cancer Research.

“This discovery will allow physicians to individualize treatment and observation plans for prostate cancer patients,” says Timothy Roth, M.D., a Mayo Clinic urology resident and lead author of the study. “Being able to tell a patient his specific risk after surgery, and perhaps even prior to surgery, will be a huge step forward.”

Researchers have reported new insight into the pathology underlying a recently identified neurological disorder that strikes middle-aged adults that is caused by alterations in the same gene that causes fragile X syndrome. “Fragile X tremor/ataxia syndrome” (FXTAS) overwhelmingly affects males, usually in their 50s, causing Parkinson’s-like symptoms and cognitive decline. In contrast, fragile X syndrome manifests itself from birth and is the most common form of X-linked mental retardation.

In two related papers, researchers report studies revealing how FXTAS might arise from malfunction of the same gene that causes fragile X syndrome.

A prominent problem in AIDS is a form of dementia that robs one’s ability to concentrate and perform normal movements. Scientists at the Burnham Institute for Medical Research (Burnham) have discovered how HIV/AIDS disrupts the normal replication of stem cells in the adult brain, preventing new nerve cells from forming.

Drs. Stuart Lipton, Marcus Kaul, Shu-ichi Okamoto and their colleagues uncovered a novel molecular mechanism that inhibits stem cell proliferation and that could possibly be triggered in other neurodegenerative diseases as well.

A normally functioning adult human brain has the ability to partially replenish or repair itself through neurogenesis, the proliferation and development of adult neural progenitor/stem cells (aNPCs) into new nerve cells.