Sentences with phrase «of cohesin»

Since actual cohesion defects will cause mitotic failure (which most surely results in cell death), most of cohesin - associated diseases are believed to be caused by misregulation of the complex's non-canonical functions in replication / transcription.

The last stage in the life of a cohesin ring is its removal from centromeres, a tightly regulated process, which involves proteolytic cleavage of cohesin's Scc1 / Rad21 subunit (see Figure 2).

However, a small but very important fraction of cohesin molecules, which is located at the chromosomes» centromere regions, remains protected from this removal mechanism in prophase.

Stage - specific binding profiles of cohesin in resting and activated B lymphocytes suggest a role for cohesin in immunoglobulin class switching and maturation.

«By knowing which of the Cohesin / CTCF bound sites are coming together in physical proximity, we started to go from a linear view of the genome to sets of looping interactions, which led us to these domains, these super enhancer domains, where gene expression enhancement is contained within the loop,» says Jill Dowen, a postdoctoral researcher in Young's lab.

Gamze Gunal (Jessberger, TUD)-- «Stage - specific binding profile of cohesin in resting and switch - activated B lymphocytes» (2013)

His research currently focuses on determining the mechanisms and consequences of cohesin gene inactivation in human cancer.

CdLS is known to result from mutations in subunits or regulators of cohesin, a group of linked proteins necessary for cell division and other cell processes.

So, it's as if there's a chromosome - specific failure of the cohesins to dissolve.

Not exact matches

«This also raises the possibility that mild mutations in cohesin genes may be the cause of some fraction of congenital heart defects in the general population,» she says.

Research coordinated by Osaka University has now shown that the nuclear protein complex cohesin must be expressed at sufficient levels in the early mouse brain to control gene regulation and allow development of healthy neuronal networks and behavioral characteristics.

«Now, through our new study, we show that lowering levels of a particular cohesin protein called Rad21 in embryonic zebrafish produces similar types of heart defects to those found in people with CdLS,» Associate Professor Horsfield says.

«Regulator of chromosome structure crucial to healthy brain function and nerve development: Cohesin protein identified as key to control of chromosome structure underlying nerve cell network formation.»

«We also found that reduced cohesin led to changes in the expression of genes involved in nerve cell development and the response to an immune signaling protein,» corresponding author Toshihide Yamashita says.

Unless sufficient cohesin was present in the developing mouse brain, the researchers showed that the regulation of a number of genes was disrupted, leading to neuronal defects and increased anxiety.

Cohesin encircles the DNA strand as a ring does around a piece of string, and the protein complexes that replicate DNA can pass through the ring without displacing it.

By only analysing DNA sequences that bind to cohesin, roughly one per cent of the genome, it would allow us to analyse an individual's mutations and make it much easier to conduct studies to identify novel harmful mutations,» Martin Enge concludes.

Gabriela Cabral, a PhD student in the lab of Alex Dammermann at the Center for Molecular Biology of the University of Vienna, explains: «Many people thought that centrioles are held together by the same glue as chromosomes, a substance called cohesin, which is destroyed during cell division.

Cohesins are protein complexes that bind two straps of DNA and are implicated in its repair, replication and recombination, as well as in its chromosomal stability, transcription regulation, stem - cell pluripotency, and cell differentiation.

In previous studies, researchers proved in mice that genes of the meiotic cohesin complex produce various degrees of infertility in mice.

CSIC researcher adds: «We have confirmed that mutation is found in both copies of the gene, one inherited from the father and the other one inherited from the mother, in the four women affected by the disease, causing an absolute absence of STAG3 protein and meiotic cohesin complex in these women.

The proteins Cohesin (blue lines) and CTCF (purple blocks) act as the purse strings of DNA «goody bags» (gray lines).

According to our current understanding, cohesin is already loaded onto DNA (along the entire length of the decondensed one - chromatid chromosome) in telophase, i.e. only minutes after chromosome segregation, by opening / closing its Smc1 - Smc3 interaction site (or «entry gate»).

That poses an obvious problem during S phase: While DNA replication machineries («replisomes») zip along the chromosomes trying to faithfully duplicate the entire genome in a matter of just a couple of hours, they encounter — on average — multiple cohesin rings that are already wrapped around DNA.

This means that cohesin has at least the potential to influence a whole bunch of other chromosomal events, like DNA replication, gene expression and DNA topology.

And while this feat should already be enough to warrant devoting a whole blog post to cohesin, you will shortly realize that this complex also performs a myriad of other functions during the cell cycle, which really makes it «one ring to rule them all».

It is important to mention that cohesin also has a very unique role in meiosis where it not only coheses sister chromatids but also chromosomal homologs (the two maternal / paternal versions of a chromosome, each consisting of two sisters, which themselves are cohesed).

Because of its pleiotropic functions, defects in human cohesin biology can cause a number of clinically relevant issues.

More specifically, we have been studying the roles of the condensin and cohesin complexes in 3D genome organization in the fission yeast, mouse and human systems.

After twenty years of research, the cohesin complex still manages to surprise us regularly, as new functions in new areas of cell cycle regulation come to light.

Currently, extensive research is conducted to better understand the role of certain cohesin mutations in cancers such as glioblastoma, or Ewing's sarcoma.

Cohesin forms small topological chromatin domains of approximately 100 kb, while condensin organizes 300 kb — 1 Mb domains.

Soon after cohesin was described as this guardian of sister chromatid cohesion, it also became clear that there is just more to it.

These studies demonstrate that the two important protein complexes, condensin and cohesin, are both essential for the assembly of the functional genome architecture, but their roles in the 3D genome organization (gene contacts and topological domain organization) are significantly different.

Studying cohesin has, of course, not only academic value.