Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.

[Q]: FK506 binding protein 6, also known as FKBP6, is a human gene.
[A]: In what living being can FKBP6 be found?

[Q]: Nuclear receptor co-repressor (N-CoR) plays important role in transcriptional control mediated by several tumor suppressor proteins. Recently, we reported a role of misfolded-conformation dependent loss (MCDL) of N-CoR in the activation of oncogenic survival pathway in acute promyelocytic leukemia (APL). Since N-CoR plays important role in cellular homeostasis in various tissues, therefore, we hypothesized that an APL like MCDL of N-CoR might also be involved in other malignancy. Indeed, our initial screening of N-CoR status in various leukemia and solid tumor cells revealed an APL like MCDL of N-CoR in primary and secondary tumor cells derived from non-small cell lung cancer (NSCLC). The NSCLC cell specific N-CoR loss could be blocked by Kaletra, a clinical grade protease inhibitor and by genistein, an inhibitor of N-CoR misfolding previously characterized by us. The misfolded N-CoR presented in NSCLC cells was linked to the amplification of ER stress and was subjected to degradation by NSCLC cell specific aberrant protease activity. In NSCLC cells, misfolded N-CoR was found to be associated with Hsc70, a molecular chaperone involved in chaperone mediated autophagy (CMA). Genetic and chemical inhibition of Lamp2A, a rate limiting factor of CMA, significantly blocked the loss of N-CoR in NSCLC cells, suggesting a crucial role of CMA in N-CoR degradation. These findings identify an important role of CMA-induced degradation of misfolded N-CoR in the neutralization of ER stress and suggest a possible role of misfolded N-CoR protein in the activation of oncogenic survival pathway in NSCLC cells.
[A]: Which is the receptor for substrates of Chaperone Mediated Autophagy?

[Q]: Mutations of the alpha-synuclein gene have shown to be relevant in some rare families with autosomal dominant Parkinson's disease (PD). Furthermore, alpha-synuclein protein is a major component of the Lewy bodies also in sporadic PD patients. Increased levels of wildtype alpha-synuclein in the cell leads to increased intracellular hydrogen peroxide levels and causes death of dopaminergic neurons in rat primary culture. Subsequently, oxidative stress has been directly linked with alpha-synuclein aggregation in vitro. This raises the question whether increased alpha-synuclein expression might be linked to higher susceptibility to PD and whether alpha-synuclein promoter polymorphisms are associated with PD. Here, two polymorphisms (-116C>G and -668T>C) of the alpha-synuclein promoter defining four haplotypes have been characterized in 315 German PD patients. The influence of the four haplotypes on gene expression was studied by CAT reporter gene assays in neuronal SK-N-AS cells. The -668C/-116G haplotype revealed significant higher CAT expression than the -668T/-116G or the -668T/-116C haplotype, respectively. Although the -668C/-116G haplotype was more common in PD patients, this difference was not significant.
[A]:
Which is the primary protein component of Lewy bodies?