The interest in using primary cells for cell-biology research has gained prominence in recent years due to factors such as cell line contamination (Kaur G, 2012). What made primary cells lose their popularity in the first place is partly due to the rigorous and arduous process associated with primary-cell cultivation. So why is primary-cell cultivation so difficult?

It’s no secret that scientific research is becoming less of a priority to the federal government. For two decades, research and development (R&D) funding has remained stagnant or dropping, despite increases to the overall federal budget. With a growing population of scientists entering the field, a lack of funding generates a hyper-competitive and stressful funding climate. For those looking to secure funding for the first time, or simply curious about how science is funded, this post serves as an introductory guide.

The G2/M cycle checkpoint prevents cells with genomic DNA damage from entering mitosis (M phase). The main safeguards conferred by this checkpoint is to ensure that DNA is free of major lesions or replication errors, and there are enough organelles, metabolites, and other cellular cargo in the parent cell prior to division so the daughter cells can be adequately provided for once mitosis is complete. Failures at this checkpoint are associated with aberrant cellular growth and cancer progression.

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. Stopping cell cycle progression allows the cell enough time to attempt to repair any DNA or cellular damage, and if all else fails, to induce apoptosis to prevent risk to the entire organism.

ABclonal Technology provides a wide selection of cell cycle checkpoint antibody products for every phase of a cell's life. Please see a small sample of our offerings below.

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?

The G1/S cell cycle checkpoints control whether eukaryotic cells enter the S phase (synthesis phase) of DNA synthesis after having properly completed the G1 phase to ensure the cell has enough energy and resources to begin DNA replication. 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 cyclin D is down-regulated by down-regulation of protein expression and phosphorylation-dependent degradation. Without a proper G1/S checkpoint, the cell could arrest or potentially undergo aberrant processes that could lead to disease states such as cancer.