Recent Posts

Can You Guess How Much Darwin Worked?

Posted by Michele Mei on Apr 21, 2019 7:34:18 PM

Being perpetually busy has become a status symbol in academia –and it’s counterproductive.

In this day and age, we are trained to believe that the more you work, the more you get done, and the further ahead you get. In academia, researchers place a lot of pressure on themselves to work around the clock. Whether it’s experiments, teaching, papers, or grants, it seems like there’s always more to be done. Consequently, the lack of work-life balance, work-induced stress, and burnout has become a pervasive problem in academia.

G2/M Cell Cycle Checkpoint Antibody

Posted by Panyue (Penny) Hao on Apr 9, 2019 3:16:32 PM

The G2/M cycle checkpoint prevents cells with genomic DNA damages from entering mitosis (M phase). The Cyclin B-CDK1 complex plays an important regulatory role during the G2 transition, at which time CDK1 is maintained inactivated by the tyrosine kinases Wee1 and Myt1. When the cells enter the M phase, the kinase Aurora A and the cofactor Bora act together to activate PLK1, which in turn activates the activity of phosphatase CDC25 and downstream CDC2, effectively driving the cells into mitosis. When the DNA is damaged, it activates the DNA-PK/ATM/ATR kinase and eventually inactivates the Cyclin B-CDK1 complex.

Why doesn’t the heart get cancer?

Posted by Michele Mei on Mar 29, 2019 1:41:43 PM

In some ways, the heart is quite a vulnerable organ. Cardiac complications such as heart attack, cardiac arrest, or heart failure are common. But interestingly, of the many diseases that may affect the heart, cancer is not one of them. For example, we often hear about cancer in the prostate, breast, colon, skin, etc., but rarely of the heart. How is this vital organ different?

G1/S Cell Cycle Checkpoint Antibody

Posted by Panyue (Penny) Hao on Mar 29, 2019 11:09:52 AM

The G1/S cell cycle checkpoints control whether eukaryotic cells enter the S phase (synthesis phase) of DNA synthesis through the G1 phase. Two cell cycle kinase complexes, CDK4/6-Cyclin D and CDK2- Cyclin E, work together to relieve the inhibition of dynamic transcriptional complexes containing retinoblastoma protein (Rb) and E2F. In cells undefined during the G1 phase, hypophosphorylated Rb binds to the E2F-DP1 transcription factor and forms an inhibitory complex with HDAC, thereby inhibiting downstream key transcriptional activities. Clear entry into the S phase is achieved by continuous phosphorylation of Rb by Cyclin D-CDK4/6 and Cyclin E-CDK2, which separates the transcription factor E2F from the inhibitory complex and allows transcription of the gene required for DNA replication. After the growth factor disappears, the expression level of cylin D is down-regulated by down-regulation of protein expression and phosphorylation-dependent degradation.

New and Old Techniques to Study Protein-DNA Binding

Posted by Michele Mei on Mar 11, 2019 12:28:22 AM

Proteins known as transcription factors play a crucial role in gene regulation by activating, enhancing, and even silencing a gene’s expression.  Many textbooks and resources compare transcription factors (TFs) to something like an on/off switch for gene transcription. However, it is a bit more complicated than just turning gene expression on or off. Various properties (e.g. binding affinity, specificity, and genetic variance of binding sites) impact the binding of TFs to DNA, thereby altering gene expression. To study transcription and how it is regulated, scientists study TF-DNA interactions on a genome-wide level. 

Tumor Immunology Targets

Posted by Panyue (Penny) Hao on Mar 5, 2019 12:11:55 PM

A healthy immune system requires a series of checkpoints to ensure self tolerance and prevent damage to other tissues during immune response. Binding of costimulatory signal transduction molecules (such as CD28, ICOS, GITR) on T cells to their receptors (such as CD80/CD86, ICOSL, GITRL) on antigen presenting cells (APCs) may contribute to T cell activation. However, in some states, inhibitory signals of T cell activation and response occur during the involvement of T cell receptors. These signals are generated by proteins involved in immune checkpoints (eg, PD-1, CTLA-4, TIM-3, and LAG3). Usually PD-1 and CTLA-4 immunological checkpoint proteins are upregulated in T cells infiltrating tumors and bind to their respective ligands, PD-L1 (ligand B7-H1)/PD-L2 (ligand B7- DC) and CD80/86, and down-regulate T cell responses. Immunological checkpoint ligands are often upregulated in cancer cells as a means of evading immune detection. Therefore, immunotherapy by blocking immunological checkpoint protein activation of anti-tumor immunity has become a popular research subject for cancer therapy.