Autophagy & Apoptosis

Apoptosis

the programmed cell death

Apoptosis is a highly regulated process in multicellular organisms. There are two initiation pathways induce either by an internal trigger, intrinsic pathway, like cell stress or an external trigger, extrinsic pathways, e.g. specific signaling from surrounding cells. The underlying mechanism induced by both pathways is the activation of initiator caspases and the downstream activation of executioner caspases which are specific enzymes/proteases degrading proteins indiscriminately.

The program follows very characteristic changes including blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, chromosomal DNA fragmentation and RNA decay. The formation of apoptotic bodies prevent the release of cellular content onto surrounding cells and are finally removed by phagocytic cells.

Apoptosis represents a very important process druing an organism's life cycle e.g. during development and homeostatsis. Defects in the apoptotic pathway have been linked to a wide range of diseases. The regulation of the apoptotic pathways by proteins promting or inhibiting apoptosis thus is a critical equilibrium to prevent atrophy caused by extensive apoptosis or uncontrolled cell proliferation resulting in diseases such as cancer.

The protein p53 has sigificant impact on that critical equilibrium. This tumor-suppressor protein usually accumulates when DNA is damaged due to a chain of biochemical factors. While repairing p53 stops the cell from replicating by stopping the cell cycle at G1 or interphase. This Process gives the cells time to repair damage, however it will induce apoptosis if damage is extensive and repair efforts fail.

p53 - tumor supressor

PROGEN´s trusted p53 antibodies for cell cycle research and tumor analysis

Browse our p53 Antibodies

suitable for
ICC, IF, IP, WB

Browse p53 Antibodies

As mentioned above p53 proteins can stop cells from replicating and induce apoptose in highly damaged cells e.g. tumor cells which makes them effective tools against cancer. Unfortunately p53 is typically mutated in tumor cells wich leads to an abnormal response and no apoptosis induction. Usually this Mutations occur in the central DNA-binding Domain, causing a dominant negative effect for the protein and making it impossible to bind DNA or react as a transcription factor. As a result accumulating wild type p53 are inactivated and without regulation of cell cycle or apoptosis, potentially rogue cells can divide erratically.

Therefore PROGEN provides excellent markers for wild-type and mutant human p53. Our Antibodies are avaiable in different antigen and application formats, staining approx. 60% of investigated carcinoma including several positive targets like:

• Tumor of lung, breast, colon, stomach, esophagus, pancreas, urinary bladder and
  testis
• Head and neck
• T-cell Leukemia
• Non-Hodgkin-Lymphoma
• Melanoma
• Sarcoma

Because of the important role of p53 in tumor suppression, and its mutations benefitting tumorigenesis, it is an important target in cancer therapy. Gene therapies are studying the effect of a transfer of a correct gene copy into the organism, others approach the issue with immune therapies against the defect p53 gene. Some researches could show that with the help of altered AAV, cells with mutated p53 could be eliminated. For more information towards AAV, feel free to check out our AAV Category.

PROGEN's reliable p53 antibodies

Our Antibodies are highly puplished and used in many publications.
Check out our references below to read furthermore or convince yourself by buying a sample size set!

Publications

1. Ohtaké, S. et al. Precancerous foci in pleomorphic adenoma of the salivary gland: recognition of focal carcinoma and atypical tumor cells by P53 immunohistochemistry. J. Oral Pathol. Med. 31, 590–7 (2002).
2. Homann, N. et al. Overexpression of p53 in tumor-distant epithelia of head and neck cancer patients is associated with an increased incidence of second primary carcinoma. Clin. Cancer Res. 7, 290–296 (2001).
3. Vispo, N. S., Araña, M. J., Chinea, G., Ojalvo, a G. & Cesareni, G. Characterisation of epitopes on human p53 using phage-displayed peptide libraries: insights into antibody-peptide interactions. Hybridoma 18, 251–255 (1995).
4. Petersen, G., Song, D., Hugle-Dorr, B., Oldenburg, I. & Bautz, E. K. Mapping of linear epitopes recognized by monoclonal antibodies with gene-fragment phage display libraries. Mol Gen Genet 249, 425–431 (1995).
5. Bártek, J. et al. Immunohistochemical analysis of the p53 oncoprotein on paraffin sections using a series of novel monoclonal antibodies. J. Pathol. 169, 27–34 (1993).