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More at http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/C/Codons.html

August1-2, 2014

Organised By

Centre of Excellence in Bioinformatics
Bioinformatics Infrastructure Facility
Department of Biochemistry
University of Lucknow
Lucknow-226007

Course Contents

Molecular Modeling
Homology Modeling
Molecular Docking
Post-structural Analyses

Molecular Dynamics (MD)
Simulation
Linux Introduction
Gromacs Installation

MD Simulation of Protein ligand complex
Analyses of MD
Trajectories
Visualization of Dynamic
complexes

Important Dates

Registration Begins June 25, 2014
Registration Closes July 25, 2014

Brochure : www.lkouniv.ac.in/conference/Brochure_August,%202014.pdf

The program utilizes tBLASTn and BLASTn algorithms to map genes from the reference genome (the annotated strain) to the new sequence (the unannotated strain). The goal is to annotate the majority of the new genome’s genes in a single step. ORFs present in the target genome and absent from the reference genome are also identified; these ORFs can be further analyzed using BLAST, VGO and BBB. Afterwards, they can either be accepted for/rejected from annotation. GATU can handle multiple-exon genes as well as mature peptides. Although it was designed for use with viral genomes, GATU can also be used to help annotate larger genomes (ie. bacterial genomes).

The output is saved in GenBank, XML, or EMBL file format.

Address of the bookmark: https://virology.uvic.ca/help/tool-help/help-books/genome-annotation-transfer-utility-gatu-documentation/

Address of the bookmark: http://www.mdpi.com/2073-4425/3/3/423

Most people who have a balanced translocation have the right amount of chromosome material but it has been rearranged in some way. This may happen if two chromosomes swap pieces (a reciprocal translocation). In other cases two whole chromosomes may become stuck together (a Robertsonian translocation). This page describes what happens when someone has a reciprocal translocation.

Reciprocal chromosomal translocations occur following double-strand breaks (DSBs) in DNA when a section of one chromosome is exchanged with that of another, non-homologous chromosome. These exchanges may produce a dysfunctional fusion gene that disrupts cell growth and survival pathways, such as the translocations seen in leukemia and childhood sarcomas.

Chromosomal translocations have been well studied in cancer cell lines which are associated with two types of cancer, acute myeloid leukemia and Ewing's sarcoma, but determining how they contribute to cancer development is complicated by additional mutations and altered gene expression profiles in these cultured cells. Now, Juan Carlos Ramirez, head of the Viral Vector Facility at the Fundacion Centro Nacional de Investigaciones Cardiovasculares (CNIC) and his colleagues Raul Torres at CNIC and Sandra Rodriguez-Peralez at the Spanish National Cancer Center (CNIO) in Madrid, Spain have used a new genome editing tool, CRISPR-Cas9, to induce chromosomal translocations for the first time in a human cell line and in primary cells. The study's authors conclude by stating that the use of this technology will allow for the clarification of how and why chromosomal translocation occurs, which without doubt will allow new anti-cancer therapeutic strategies to be tackled.

Using RNA-Guided Endonuclease (RGEN) technology or CRISPR/Cas9 genome engineering technology, CNIO and CNIC researchers have shown that it is possible to obtain such chromosomal translocations. The CRISPR-Cas9 system is extremely simple to introduce a cut at the desired locus, easier to design, and cheaper than many other systems. Using the CRISPR-Cas9 system, Ramirez and his colleagues reproduced the translocations observed in Ewing’s Sarcoma (ES) and Acute Myeloid Leukemia (AML) patient cell lines in HEK293 cells and also generated the ES translocation in human mesenchymal stem cells and the AML translocation in umbilical cord blood cells.

By focusing on chromosomal translocation without the confounding characteristics of established cell lines, these new cells lines should help answer the fundamental question of what causes a cell to become cancerous. Ramirez and his team now look forward to modeling other chromosome translocations in a variety of cell types.

Reference:

http://en.wikipedia.org/wiki/Chromosomal_translocation

http://www.nature.com/ncomms/2014/140603/ncomms4964/abs/ncomms4964.html

Brief description: We are looking for suitable candidates in the area o computational biology/bioinformatics/genomics or related field for next-generation sequencing (NGS) data analysis for small-RNAs, RNA-Seq and targeted resequencing of plants and associated organisms. We are an interdisciplinary group where projects equally involve bioinformatics and systems biology (specially microarrays and next-generation sequencing (NGS) data analysis and its use), along with plant molecular biology, genetic engineering, field biology, and analytical plant chemistry for understanding response of plants to biotic stresses.

Essential qualification: MSc/BTech/MTech/PhD (or other suitable qualification) in disciplines preferable to bioinformatics, computational biology, computer application (or equivalent)/ ‘Advance Post-Graduate Diploma in Bioinformatics’. Proficiency in programming languages (such as Perl, C++) and/or statistics (proficient in R for example) is compulsory.

Desirable qualification: Experience in the field of genomics e.g. microarray analysis, NGS, genome annotation, database development and management, software development, systems and network biology (or related fields) will be preferred.

Application process: Applications should contain CV along with brief description (maximum 1 page) of research conducted (highlighting skills and experience) till now. Applications should be sent by e-mail to Shree Prakash Pandey, Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur Campus, WB, India within 14 days of this advertisement.

E-mail: sppiiserkol@gmail.com, sppandey@iiserkol.ac.in

Advertisement:

http://www.iiserkol.ac.in/announcements/adverts/671-advt_ra_shree_prakash_july_2014

Address of the bookmark: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4783527/

Scientists with a long-running Framingham Heart Study looked at 1,932 people (examination of about 1.5 million markers of genetic variations), comparing unrelated friends to unrelated strangers. They found that friends shared about 1% of their genes — a percentage much higher than those shared with strangers.This new findings made it clear that people have more DNA in common with those who are selected as friends than with strangers in the same population. 

The genes that lined up the most were olfactory genes, which deal with smell. The ones that lined up the least were immune system genes. The researchers weren't sure why that happened :/. Olfactory genes might be a straightforward explanation: People who like the same smells tend to be drawn to similar environments, where they meet others with the same tendencies.

Reference:

http://www.pnas.org/content/111/Supplement_3/10796.full

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