As we’ve seen over these past few months, a SARS-CoV-2 infection can result in widely different manifestations and severities in the subsequent course of the disease it causes, COVID-19. Many of those infected by SARS-CoV-2 experience a mild to severe illness, with symptoms that include fever, shortness of breath, cough, and fatigue that appear roughly 2-14 days after exposure to the virus. On the other hand, some individuals infected with the virus will remain asymptomatic.
ABclonal has developed over 12,000 high quality antibody products since its inception in 2011. With this significant and time-tested experience, you can rest assured that ABclonal is relentless in its focus on the production and development of quality antibodies. Let’s further our understanding of antibodies by taking a more in-depth look at their structure, function, and uses in research.
In a previous article, we explored the differences between rabbit and mouse antibodies as well as the biology behind rabbit antibody superiority. But after choosing the host, the type of technology used to produce the antibody is important too. Here, we explore some of the rabbit monoclonal antibody technologies available in the current market.
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.
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.
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.