The EMBO Journal

Researchers from The University of Osaka have found that the rat brain differs from other mammals in the proportion of upper and deep layer neurons in the cortex. This change likely arises from differences in the timing of signaling pathways during early brain development. Importantly, this identified mechanism may have future applications in regenerative medicine for developmental and neurological disorders.

Researchers at The University of Osaka used a range of cellular techniques to show that the histone protein CENP-A can be deposited into centromeres by two independent pathways. By identifying that CENP-C can substitute for Mis18C in binding to the chaperone HJURP to prompt CENP-A deposition, they showed that there is redundancy in the process of specifying the location of the centromere on chromosomes, which is essential for mitosis and meiosis.

Researchers are one step closer to finding a common target for treating ALS - a fatal neurodegenerative disease that causes progressive muscle weakness.

New research suggesting a link between motor protein Kif23 and microcephaly may be the key to developing more effective treatments for this condition.

Researchers led by Osaka University used cryogenic electron microscopy to analyze the atomic structure of the centromeric region of the chromosome, essential for cell division. A protein called CENP-A marks the centromere; the researchers showed that during interphase, CENP-A is bound by a protein called KNL2 to maintain the location of the centromere. During mitosis, KNL2 is replaced by CENP-C, allowing correct formation of the kinetochore complex for cell division.

Scientists found out why people with Zellweger syndrome also get sick with genetic disorders linked to dysfunctions of the cilia or the cell’s “antenna.”

Scientists have discovered non-coding RNA has a novel role to fine-tune gene expressions during stress recovery, getting closer to uncovering a 30-year-old nuclear mystery.

A recent study, affiliated with South Korea's Ulsan National Institute of Science and Technology (UNIST) has discovered that restoring a gene altered in Down syndrome called the Down syndrome critical region 1 (DSCR1) rescued adult neurogenesis and learning and memory defects in a Down syndrome mouse model (Ts65Dn).

Korean researchers have verified the correlation between Animals’ sensory nerve activation and behavioral changes caused by insulin secretion in a feeding state. The result provided a clue to identify the causes of unusual sensory organ changes due to insulin-related metabolic syndrome such as diabetes.