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Rhodium Interaction with Human NRG1 Gene of Schizophrenia
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Abstract - Rhodium (II) acetate [Rh2 (O2CCH3)4] could be used as an indicator for single nucleotide polymorphism (SNPs) involved in the onset of schizophrenia. Rhodium (Rh1) has affinity to make covalent interactions with neuregulin (NRG1) gene at SNPs mutation. Binding effects of Rh1 has been studied under different molar concentrations at different time periods. In this study we used Rh1 to evaluate its interaction with NRG1 gene in Schizophrenic patients of Pakistan. Rh-NRG1 adduct were amplified by PCR and visualized on agarose gel electrophoresis. Here we show Rh1 binding with NRG1 gene was inhibited with increasing concentration ranges from 0.5 -3µM. It has been noted that upon binding with NRG1 gene Rh1 decreased the mobility and intensity of the DNA bands. Noticeably Rh1 didn’t inhibit the activity of Mun1 restriction enzyme having specific CAAA cleavage site. After the digestion of NRG1 gene having SNPs mutation combining with Rh1 proves its covalent binding only with Guanine or Thymine and not with Adenine or Cytosine. This is a novel study that shows rhodium can covalently binds with human dsDNA and can inhibit its amplification. The effect of Rh1 to target different SNPs mutations (normally occurs in genetic diseases such as schizophrenia) can be identified by using this technique. There are variations between human populations, so a SNP allele that is common in one geographical or ethnic group may be much rarer in another, and Rh1 can act as a useful tool to identify SNPs of schizophrenic genes.
Philippine Association of Institutions for Research, Inc.
Title: Rhodium Interaction with Human NRG1 Gene of Schizophrenia
Description:
Abstract - Rhodium (II) acetate [Rh2 (O2CCH3)4] could be used as an indicator for single nucleotide polymorphism (SNPs) involved in the onset of schizophrenia.
Rhodium (Rh1) has affinity to make covalent interactions with neuregulin (NRG1) gene at SNPs mutation.
Binding effects of Rh1 has been studied under different molar concentrations at different time periods.
In this study we used Rh1 to evaluate its interaction with NRG1 gene in Schizophrenic patients of Pakistan.
Rh-NRG1 adduct were amplified by PCR and visualized on agarose gel electrophoresis.
Here we show Rh1 binding with NRG1 gene was inhibited with increasing concentration ranges from 0.
5 -3µM.
It has been noted that upon binding with NRG1 gene Rh1 decreased the mobility and intensity of the DNA bands.
Noticeably Rh1 didn’t inhibit the activity of Mun1 restriction enzyme having specific CAAA cleavage site.
After the digestion of NRG1 gene having SNPs mutation combining with Rh1 proves its covalent binding only with Guanine or Thymine and not with Adenine or Cytosine.
This is a novel study that shows rhodium can covalently binds with human dsDNA and can inhibit its amplification.
The effect of Rh1 to target different SNPs mutations (normally occurs in genetic diseases such as schizophrenia) can be identified by using this technique.
There are variations between human populations, so a SNP allele that is common in one geographical or ethnic group may be much rarer in another, and Rh1 can act as a useful tool to identify SNPs of schizophrenic genes.
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