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Scientist
1407
Thermotolerant photosynthetic organisms endure worsening climate conditions such as increased temperatures and higher levels of CO2. These novel organisms maintain photosynthetic activity and growth under a wide temperature range (15-45oC) as opposed to their wild-type counterparts. Thermotolerant...

Thermotolerant photosynthetic organisms endure worsening climate conditions such as increased temperatures and higher levels of CO2. These novel organisms maintain photosynthetic activity and growth under a wide temperature range (15-45oC) as opposed to their wild-type counterparts.

Thermotolerant organisms also exhibit higher transparency to light. Photosynthetic efficiency is maintained even though they produce and utilize less chlorophyll molecules; therefore less surface area is required for optimal cultivation. Furthermore, increased CO2 concentrations are preferable for thermotolerant organisms’ efficient photosynthesis.

The innovative solution discovered at The Weizmann Institute, involves replacement of 1-2 amino acid residues in a protein motif within the D1 protein subunit of Photosystem II (the protein complex responsible for the conversion of solar energy to a useful form of energy by photosynthesis). Such a solution has the potential to provide platforms for food production and sustainable energy in regions with harsh climate conditions that until today, were deemed unfit for cultivation.

Applications


  • Bacterial platform to produce biomass or materials (e.g. nutraceuticals) in higher temperatures and higher CO2.
  • Food and biofuel production: adaptation of crops to harsh climates.

Advantages


  • Enhanced Thermal stability and plasticity of the modified organisms to a much broader range than observed for the native organisms.
  • Greater Light penetration (e.g. in ponds) without losing photosynthetic efficiency - thermotolerant organisms maintain efficient activity with less chlorophylls thus allowing greater transmission of light to deeper spaces.
  • Thermotolerant organisms withstand high CO2 concentrations.

Technology's Essence


Professor Avigdor Scherz and his team focused on the sequences of the two major protein subunits D1 and D2 found in all purple bacteria PSII reaction centers. Two sites, D1-209 and D1-212, were found to show consistent changes between mesophilic, thermotolerant and thermophilic organisms including cyanobacteria, algae and green plants.

The sites are positioned in a GXXXG-like structural motif (where G denotes small residues such as Gly, Ala, Ser, Cys and Thr) typical of helix-helix interactions. The motif was found at the points of closest contact between the two major protein subunits, D1 and D2. It was shown that mutations in the amino acids within the identified GXXXG-like motif  result in modification of the local flexibility of the reaction center and, consequently, in the induction of thermophilic behavior.

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  • Prof. Avigdor Scherz
1451
A monoclonal antibody against GluR3B, a peptide found in epilepsy patients, and especially in patients suffering from intractable, resistant forms of the disease, could be used in diagnosis kits as well as in drug development for this form of "autoimmune epilepsy".

A monoclonal antibody against GluR3B, a peptide found in epilepsy patients, and especially in patients suffering from intractable, resistant forms of the disease, could be used in diagnosis kits as well as in drug development for this form of "autoimmune epilepsy".

Applications


1. Producing a new kit for epilepsy patients, able to detect GluR3b Ab's and thus GluR3-mediated neuropathology
The anti GluR3B monoclonal Ab could be used for developing a new diagnostic kit to detect neuropathogenic human anti-GluR3B in serum and CSF of patients with epilepsy. The patient's GluR3B Ab's would compete and displace the GluR3B mAb's of its ligand: the GluR3B peptide. The presence of GluR3B Ab's in a patient, would indicate that autoimmunity against GluR3 may underlie the patient's neuropathology and a) would suggest the initiation of an immune-based therapy b) prevent useless and dangerous brain surgery c) prevent non-effective medication.

2. Drug design for GluR3-mediated neuropathology
The unique GluR3B monoclonal antibody could be used to screen a potential drug for 'Autoimmune Epilepsy'. The GluR3B monoclonal antibody could be used to screen for a molecule (i.e. Anti-idiotypic antibodies) that would block the GluR3 autoantibodies and their detrimental neuropathological effects.

3. Research tool for a kaleidoscope of purposes, including:

  • Detection of the GluR3 glutamate receptor subtype on various target cells.
  • Studies of the properties of the Glutamate/AMPA receptor subtype 3.
  • Studies of the Glutamate-liked agonist activity of the GluR3B monoclonal antibody, and of the GluR3 receptor ion channel gating properties.
  • Production of an animal model of 'Autoimmune Epilepsy'.
  • Studies of neuronal death caused by binding of the GluR3 autoantibody to glutamate/AMPA receptors.
  • Studies of behavioral impairments caused by binding of the GluR3 autoantibody to glutamate/AMPA receptors.

  • Technology's Essence


    Scientists from the Weizmann Institute of Science have discovered a unique anti-GluR3B monoclonal antibody Glu149/29/61.

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    • Prof. Vivian I. Teichberg
    • Prof. Vivian I. Teichberg
    1033
    A novel diagnostic test to identify individuals with increased risk of lung cancer. Lung cancer is the number one killer among cancers, with 160,000 deaths/year in the USA and 1.6 million/year worldwide. Early detection of lung cancer increases 5-year survival rate from 4% to 54%. Moreover, the...

    A novel diagnostic test to identify individuals with increased risk of lung cancer.

    Lung cancer is the number one killer among cancers, with 160,000 deaths/year in the USA and 1.6 million/year worldwide. Early detection of lung cancer increases 5-year survival rate from 4% to 54%. Moreover, the National Lung Cancer Trial (NLST) showed that early detection of lung cancer by low-dose CT reduces mortality by at least 20%. Despite recommendations for low-dose CT screening for heavy smokers fulfilling the NLST criteria, compliance is low. In addition, 80 million smokers and ex-smokers in the US who do not fulfil NLST risk criteria have no recommended solution.

    The MyRepair test fulfils this unmet medical need by providing a quantitative prediction of lung cancer risk using a simple blood test. The test is based on a personalized measurement of the patient’s DNA repair capacity, a mechanism which is highly connected to the onset of cancer. Therefore, the MyRepair technology can potentially increase early detection of lung cancer and thus save lives.

     

    Applications


    A novel diagnostic test to identify individuals with increased risk of lung cancer


    Advantages


    ·         Simplicity – MyRepair is based on a simple, cost-effective blood test.

    ·         Accessibility – Compared to low-dose CT which requires specific equipment, the MyRepair test can be easily integrated in general diagnostic labs and therefore may be more accessible to a larger portion of the population.

    ·         Additional applications – Since the test is based on measuring personalized DNA repair mechanism, it can be adopted in the future for the diagnosis of additional cancer types and DNA repair related diseases.


    Technology's Essence


    Based on the strong and well documented connection between impaired capacity for DNA repair and onset of cancer, the Livneh lab invented the MyRepair Test, a method for predicting lung cancer risk, based on measuring activity of 3 DNA repair enzymes.

    Combining enzyme activities with experimental risk estimates generated MyRepair Score, which measures personalized DNA repair capacity of tested subjects.

    An epidemiological/clinical study performed in Israel, further validated in an independent UK study, demonstrated that lung cancer patients have lower MyRepair Score than healthy people. In addition, subjects who test MyRepair-positive have an 85-fold higher risk to develop lung cancer compared to the general population.

    Low MyRepair Score is a risk factor independent of smoking, and of comparable magnitude, indicating that it can be a prognostic tool for smokers, ex-smokers, and non-smokers.

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    • Prof. Zvi Livneh
    1655
    Cellular senescence is a permanent cell cycle arrest induced by damage or stress applied on proliferating cells. In a cell autonomous manner, senescence is a potent barrier to tumorgenesis and contributes to the cytotoxicity of some anti-cancer drugs. However, with age senescence cells accumulate and...

    Cellular senescence is a permanent cell cycle arrest induced by damage or stress applied on proliferating cells. In a cell autonomous manner, senescence is a potent barrier to tumorgenesis and contributes to the cytotoxicity of some anti-cancer drugs. However, with age senescence cells accumulate and promote a number of pathological conditions. Therefore the elimination of senescent cells is desired in order to prevent tumor- and inflammation- related pathologies and also to inhibit tissue ageing.
    Today, our understanding of the mechanisms regulating the viability of senescent cells is limited. It has been suggested that senescent cells are resistant to apoptosis. Therefore, senescent cells elimination may be achieved by modifying the resistance to apoptosis of these cells.
    Here the researches demonstrate the first feasible therapeutic approach that leads to eradication of senescent cells. Combination of direct induction of apoptosis in senescent cells with induction of cell death by pro-inflammatory repose induce by p21 knockdown will lead to reduction of viable senescent cells.

    Applications


    • A therapeutic impact on inflammatory and fibrotic disease
    • Therapy for age-related disease such as type 2 diabetes, Alzheimer’s disease, Atherosclerosis, cataracts, Chronic obstructive pulmonary disease (COPD), and Osteoporosis

    Advantages


    • Effective elimination of senescent cells- removal of senescent cells can prevent or delay tissue dysfunction and extend health span
    • Does not damage normal cells even at high concentrations

    Technology's Essence


    Researches demonstrated that the anti-apoptotic proteins Bcl-xL and Bcl-w level were elevated in senescence cells of both human and mouse origin. A subsequent study, in which Bcl-xL and Bcl-w were knocked down by siRNA, revealed that a combined knock down of Bcl-xL and Bcl-w had synergic effect, resulting in reduction of 50% in cell viability. Thus the increased level of anti-apoptotic proteins Bcl-xL and Bcl-w may account for the apoptotic resistance of senescent cells. p21 knockdown induced pro-inflammatory response and cell death in senescent cells.
    Overall, the researchers show that combined inhibition of the anti-apoptotic proteins Bcl-xL and Bcl-w allows specific elimination of senescent cells and might be used to treat diseases where senescent cells are present. The researchers also found that the same effect might be achieved by reducing the expression of p21 in senescent cells. Integrating both approaches propose a more effective therapy.

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    • Ph.D. Valery Krizhanovsky
    1698
    GD is an inherited metabolic disorder, affecting about 1 in 20,000 births. GD is divided into three clinical subtypes: type 1 is the most common and is characterized by bruising, fatigue, anemia, low blood platelets, and enlargement of the liver and spleen. Types 2 and 3, also called neuronopathic GD (...

    GD is an inherited metabolic disorder, affecting about 1 in 20,000 births. GD is divided into three clinical subtypes: type 1 is the most common and is characterized by bruising, fatigue, anemia, low blood platelets, and enlargement of the liver and spleen. Types 2 and 3, also called neuronopathic GD (nGD), affect 4% of GD patients and additionally include neurological symptoms. Type 1 patients can have a normal life expectancy if treated whereas type 2/3 patients do not survive to reach adulthood. Moreover, GD carriers, approximately 1% of the population, are in a major risk of developing Parkinson’s disease. Current therapies suffer from severe drawbacks in the treatment of type 1 GD and no therapy exists that effectively treat nGD. The present technology offers a novel therapeutic target for the treatment of Gaucher's disease (GD) which addresses also the neurological symptoms.

    Applications


    • Alternative treatment for type 1 GD
    • First line therapy for nGD

    Advantages


    • A novel therapy for nGD which has no treatment for the present.
    • A novel therapeutic approach for GD type 1, via a previously unknown molecular mechanism.
    • Allows the development of an orally administered treatment, far more convenient for the patients than the existing treatments.
    • Reduced costs compared to the existing therapies of ERP or BMT

    Technology's Essence


    The proposed technology is based on the discovery that RIP3 is a key player in the manifestation of GD and that inhibiting RIP3 activity is effectively ameliorating the symptoms of GD not only in the less severe type 1 but also in the neuropathic form of the disease, types 2 and 3. nGD is associated with a massive neuronal loss and elevated RIP3 levels. Inhibition of RIP3 in a mouse model of nGD resulted in a dramatic attenuation of disease signs: drastic extension of life span, no weight loss, improvements in motor coordination, reduced neuroinflammation and improved liver and spleen injuries.

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    • Prof. Anthony H. Futerman

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