Frequently Asked Questions

1. Who are we?

We are post-doctoral researchers/junior principle investigators in academic institutes and pharmaceutical companies.

2.Why is the website unique?

During the past several years, we have accumulated a large number of 'working' protocols from plasmid miniprep to antibody generation, from immunohistochemistry to transgenic mouse generation. Here we consolidate all what we have tested and present in this website. There are several other excellent online protocol websites. However, we believe ours is unique in that we only add the protocols which have been substantially tested. We mean to make this site a place you can trust.

3. Why do we do this?

Most of us just went through painful PhD/post-doc studies. We all appreciate how important it is of a 'working' protocol. We all have the experiences as trapped in particular technical difficulties month by month. We would like to share what we know and hope your experiments work at the first time so you can save more time for other things.

We will update the protocols periodically and publish PDF file for the entire website each year. Feel free to distribute the PDF file when it is available.

4. Is it a commercial website?

No.

5. Can we provide protocols?

Yes. I am sure you have a lot. Please contact us. We will add you into our collaborating team and grant you the permission to add/edit protocols.

6. Can we add comment?

We welcome comments. We also encourange discussion of any scientific/technical problems in our forum.

7. How do I cite this website?

Please cite our website as reference in your scientific publications.


Site News
New feature:
You can add comments on protocols now. Just go to any individual method page and click on the "Add a comment" link.

Highlight of the month
Autophagy hits heart

Autophagy is acutely upregulated to provide necessary nutrients during starvation for survival. Under normal condition, constitutive autophagy is critical to perform house-keeping functions to eliminate damaged organelles and dysfunctional long-lived proteins.

Ageing is associated with accumulation of dysfunctional proteins in cells. Autophagic activity is decreasing along with ageing. Studies in worms and flies show that reconstitution of autophagy can increase life span. A recent report by Taneike and colleagues explored the role of autophagy in age-related cardiomyopathy.

In heart, autophagic activity is decreasing when ageing. Taneike et al eliminated autophagy in heart by knocking out an essential gene, ATG5, specifically in heart. The researchers found deteriorated cardiac function at 10 months of age in the deficient animals compared to wild type controls. The dysfunction of autophagy causes accumulation of dysfunctional mitochondrial, reduced mitochondrial efficiency and significant oxidative damage in cardiomyocytes. More interestingly, evidence of mitochondrial damage is obvious as early as 3 months old, before cardiac remodeling and dysfunction manifest. This study points to a possibility that autophagy is critical in maintaining cardiomyocyte homeostasis and autophagy may be a target for future therapeutic design for heart failure.... Read more highlights.