Antibodies to beclin 1 may help elucidate the significance of this protein and its role in autophagy.

Autophagy is the lysosomal degradation of cell constituents. It occurs in malnutrition, enabling the body to recycle cell components to provide metabolic precursors. Autophagy is also involved in the response to pathogens and in other processes. Some aspects are summarised here.

Homozygous beclin 1-/- embryos from chimeric beclin 1+/- mice all died in early embryogenesis. This was considered to be due to defective visceral endoderm, in which beclin 1 is normally strongly expressed. Furthermore, the beclin 1+/- mice had a higher incidence of tumours (Yue et al, PNAS 2003, 100(25) pp. 15077-15082).

A review by Sun and Peng (Laboratory Medicine 2008, 39(5):287-290) emphasises the deletion of beclin 1 in 75% of human ovarian cancers, 50% of breast cancers and 40% of prostate cancers and its decreased expression in some other human cancers. The authors’ own studies lead them to conclude that beclin 1 could be a critical switch regulating the balance between autophagy and apoptosis. Thus beclin 1 might be a target for gene therapy of cancer.

Spencer et al. (J. Neurosci. 2009 29(43) pp. 13578-13588) injected a lentivirus expressing beclin 1 into the brains of alpha-synuclein transgenic mice, thereby improving cerebral pathology. They argue beclin 1 may be a novel therapeutic target for Parkinsonism and Lewy body disease.

Researchers interested in beclin 1 will find 57 different polyclonal and monoclonal anti-beclin antibodies in the Novus Biologicals antibody catalog, in addition to Beclin 2 antibodies. This impressive antibody catalog is a resource which has the potential to benefit the work of researchers involved in many spheres of ‘cutting edge’ health-related activity.

Treating cancer is a major health priority in western society. Coupled with attempts to alter unhealthy behaviour, it is hoped that better cancer treatment can reduce premature deaths.

Anti-APE1 mouse monoclonal antibodies from Novus Biologicals were antibodies used to investigate drug resistance in non-small cell lung carcinoma (Wang et al., Lung Cancer 2009, 65(3), pp. 298-304). Tumour drug resistance results in less successful chemotherapy.

Apurinic/apyrimidinic endonuclease (APE1) has a key role in the repair of DNA damage. By protecting cells from the genotoxic and cytotoxic effects of oxidising agents, APE1 counters the development of a number of pathologies.

Conversely, in the case of tumour cells, the protective effects of APE1 will have negative consequences if they result in the tumour having an increased capacity to resist anti-cancer treatment.

Wang and colleagues used anti-APE1 antibodies in immunohistochemical and Western blot studies to investigate APE1 protein expression in tumour samples from patients with non-small cell lung carcinoma. The tumours varied in their resistance to cisplatin chemotherapy. High levels of APE1 expression were seen in 83.3% of resistant tumours, but in only 8.3% of sensitive tumours. Low expression levels of APE1 correlated with longer overall survival and disease-free survival of the patients.

Further studies in a human lung adenocarcinoma cell line showed that cisplatin increased APE1 expression in these cells. Treatment of the cells with an adenoviral vector carrying APE1 siRNA (small interfering RNA) inhibited APE1 expression and increased cell sensitivity to cisplatin.

Anti-AGE antibodies are not the elixir of youth as their name might imply! They have nevertheless provided new information about Alzheimer’s disease, the major cause of dementia in old age.

Advanced glycation end products (AGE) are produced by glycation and oxidation reactions between sugars and free amino groups on proteins and amino acids. They are implicated in a wide range of pathologies. AGE can form in cooked foods. In addition, glycation reactions within the blood form endogenous AGE. High blood sugar levels favour endogenous AGE production.

Diabetes is a risk factor for Alzheimer’s. This motivated a study by Burdo et al (Neurobiol. Aging 2009, 30(12), pp. 1910-1917). The authors used anti-AGE antibodies from Novus Biologicals to detect AGE.

Firstly, they demonstrated synergistic interactions between glucose and beta amyloid peptide leading to increased AGE accumulation in cultured brain microvascular endothelial cells.

They then investigated the relationship between AGE accumulation and elevated blood glucose in transgenic mice expressing mutant human amyloid precursor protein and presenilin. These mice are a model for presymptomatic Alzheimer’s disease.

Mice that were made diabetic showed decreased cognitive functions compared to controls. This was associated with increased levels of AGE in cerebral microvessels. On the other hand, no amyloid plaques or tangles were apparent in the brains of these mice.

The role of diabetes in presymptomatic Alzheimer’s and early loss of cognitive function has thus been further elucidated with the aid of anti-AGE antibodies from Novus Biologicals. This has to be recognised as a meaningful advance in attempts to understand the connections between two conditions that have considerable impact on well being in contemporary society.