The IMPC recently exhibited at the BCS Annual Conference for the first time. The aim of attending conferences such as this is to engage with clinicians and researchers working on human disease models to raise awareness of the IMPC as a resource. The BCS Annual Conference 2018 was a great example of this and we had many interested attendees visiting the stand. Visitors ranged from researchers that had already used IMPC resources and were keen to hear updates, to those that were unaware of what we do and were interested in understanding how the IMPC may benefit their work.
To highlight how the IMPC could be used as a resource for cardiovascular research we talked attendees through the cardiovaducalr landing page.
More information on cardiovascular research and the IMPC
The cardiovascular system refers to the observable morphological and physiological characteristics of the mammalian heart, blood vessels, or circulatory system that are manifested through development and lifespan.
So far a total of 4804 genes have been tested for cardiovascular phenotypes, ranging from Increased Heart Weight to Increased Cardiac Muscle Contractility.
There have already been many studies on the cardiovascular system that have featured IMPC data and resources. A full list can be found on the cardiovaducalr landing page, and a selection of highlights listed below:
- Cardiovascular exploration integrated in International Mouse Phenotyping Consortium of new mutants for enhancer genes
- Loss-of-function mutations in co-chaperone BAG3 destabilize small HSPs and cause cardiomyopathy
- The International Mouse Phenotyping Consortium (IMPC): a functional catalogue of the mammalian genome that informs conservation
- Putative functional genes in idiopathic dilated cardiomyopathy
- Genome-wide association studies and contribution to cardiovascular physiology
- Loss of type 9 adenylyl cyclase triggers reduced phosphorylation of Hsp20 and diastolic dysfunction
- Haplo-insufficiency of Bcl2-associated athanogene 3 inmice results in progressive left ventricular dysfunction,β-adrenergic insensitivity, and increased apoptosis
- Characterization of Sgo1 expression in developing and adult mouse