Human Rights Due Diligence (HRDD) and Human Rights Impact Assessment (HRIA) Best Practices to Corporate Shared Value (CSV): a Case of British Petroleum Tangguh Project in Papua

The Tangguh Liquefied Natural Gas (LNG) Project is a planned natural gas development project located in the remote area of Berau-Bintuni Bay in Papua Province, Indonesia. British Petroleum (BP) Tangguh project aims tobe the pioneer in producing natural gas. It can be concluded that BP contributes an innovative approach, bearing in mind to sustainable development, cultural preservation and biodiversity conservation. Therefore, in each of its corporate actions, BP always integrates the value of community, partnership, consultation and corporate responsibility. It is mentioned that through experience and observation, BP as an extractive company, haveestimated the costs of not finding a better mechanism to adjust to social challenges can be higher than the costs of the uncertainties inherent in the trial of new ideas. However, according to International Non-GovernmentalOrganization (NGO), Down to Earth, BP has conducted a series of human rights violations by exploiting natural resources in Papua and restricting Papuans in enjoying their fundamental human rights. If only the BP keeps this Tangguh project in line with its aim to accommodate concerns from the affected surroundings, thus, will surely bring positive changes in BP\u27s corporate shared value

A novel brain-enriched E3 ubiquitin ligase RNF182 is up regulated in the brains of Alzheimer's patients and targets ATP6V0C for degradation

<p>Abstract</p> <p>Background</p> <p>Alterations in multiple cellular pathways contribute to the development of chronic neurodegeneration such as a sporadic Alzheimer's disease (AD). These, in turn, involve changes in gene expression, amongst which are genes regulating protein processing and turnover such as the components of the ubiquitin-proteosome system. Recently, we have identified a cDNA whose expression was altered in AD brains. It contained an open reading frame of 247 amino acids and represented a novel RING finger protein, RNF182. Here we examined its biochemical properties and putative role in brain cells.</p> <p>Results</p> <p>RNF182 is a low abundance cytoplasmic protein expressed preferentially in the brain. Its expression was elevated in post-mortem AD brain tissue and the gene could be up regulated <it>in vitro </it>in cultured neurons subjected to cell death-inducing injuries. Subsequently, we have established that RNF182 protein possessed an E3 ubiquitin ligase activity and stimulated the E2-dependent polyubiquitination <it>in vitro</it>. Yeast two-hybrid screening, overexpression and co-precipitation approaches revealed, both <it>in vitro </it>and <it>in vivo</it>, an interaction between RNF182 and ATP6V0C, known for its role in the formation of gap junction complexes and neurotransmitter release channels. The data indicated that RNF182 targeted ATP6V0C for degradation by the ubiquitin-proteosome pathway. Overexpression of RNF182 reduced cell viability and it would appear that by itself the gene can disrupt cellular homeostasis.</p> <p>Conclusion</p> <p>Taken together, we have identified a novel brain-enriched RING finger E3 ligase, which was up regulated in AD brains and neuronal cells exposed to injurious insults. It interacted with ATP6V0C protein suggesting that it may play a very specific role in controlling the turnover of an essential component of neurotransmitter release machinery.</p

A novel neuron-enriched protein SDIM1 is down regulated in Alzheimer's brains and attenuates cell death induced by DNAJB4 over-expression in neuro-progenitor cells

<p>Abstract</p> <p>Background</p> <p>Molecular changes in multiple biological processes contribute to the development of chronic neurodegeneration such as late onset Alzheimer's disease (LOAD). To discover how these changes are reflected at the level of gene expression, we used a subtractive transcription-based amplification of mRNA procedure to identify novel genes that have altered expression levels in the brains of Alzheimer's disease (AD) patients. Among the genes altered in expression level in AD brains was a transcript encoding a novel protein, SDIM1, that contains 146 amino acids, including a typical signal peptide and two transmembrane domains. Here we examined its biochemical properties and putative roles in neuroprotection/neurodegeneration.</p> <p>Results</p> <p>QRT-PCR analysis of additional AD and control post-mortem human brains showed that the SDIM1 transcript was indeed significantly down regulated in all AD brains. SDIM1 is more abundant in NT2 neurons than astrocytes and present throughout the cytoplasm and neural processes, but not in the nuclei. In NT2 neurons, it is highly responsive to stress conditions mimicking insults that may cause neurodegeneration in AD brains. For example, SDIM1 was significantly down regulated 2 h after oxygen-glucose deprivation (OGD), though had recovered 16 h later, and also appeared significantly up regulated compared to untreated NT2 neurons. Overexpression of SDIM1 in neuro-progenitor cells improved cells' ability to survive after injurious insults and its downregulation accelerated cell death induced by OGD. Yeast two-hybrid screening and co-immunoprecipitation approaches revealed, both <it>in vitro </it>and <it>in vivo</it>, an interaction between SDIM1 and DNAJB4, a heat shock protein hsp40 homolog, recently known as an enhancer of apoptosis that also interacts with the mu opioid receptor in human brain. Overexpression of DNAJB4 alone significantly reduced cell viability and SDIM1 co-overexpression was capable of attenuating the cell death caused DNAJB4, suggesting that the binding of SDIM1 to DNAJB4 might sequester DNAJB4, thus increasing cell viability.</p> <p>Conclusion</p> <p>Taken together, we have identified a small membrane protein, which is down regulated in AD brains and neuronal cells exposed to injurious insults. Its ability to promote survival and its interaction with DNAJB4 suggest that it may play a very specific role in brain cell survival and/or receptor trafficking.</p