Mass spectrometry has emerged as a highly effective analytical technique capable of detecting vast numbers of peptides in complex mixtures. This is achieved by mapping INCB28060 spectra generated from a MS experiment to a database of known or, more commonly, theoretically derived spectra to infer the peptide sequence. Exon skip splice isoforms are characterized by the peptides spanning the exon-exon junction of a novel splicing event. To detect these peptides, we generate a database containing the theoretical exon-skip junction peptides across a genome. We then use standard MS search tools to identify junction peptides that represent exon skip events in MS/MS spectra by comparison with this database. Here, we show that this approach can detect novel exon skip events in human platelets and verify a number of these at the mRNA level. We found that GDAP1 integrates into the membrane exclusively dependent on the TA-domain and not on other cytosolic domains like an N-terminal targeting sequence, the GSTdomains, or HD1. In contrast, the two TMD-containing MOM protein Mfn2 did not integrate in our assay system. A similar integration of in vitro translated TA-proteins into the MOM has previously been demonstrated in digitonin-permeabilized HeLa cells. The expansion impedes the transcription of the gene and reduces frataxin levels to a few percentage points of normal. Affected tissues are deficient in iron-sulfur cluster proteins , whose assembly is impaired as a result of inadequate handling of iron. We did not find evidence that new neurons were generated by any of the experimental intervention. The molecular environment of the spinal cord is predominantly gliogenic, but not conducive for the generation of new neurons. We assumed that VEGF provided by F3.VEGF grafts could not overcome the limitation imposed by the molecular niches in the spinal cord. Increases in the number of proliferating NG2+ glial progenitor cells and newly born oligodendrocytes can have important implications in the recovery of neurological function after SCI. Demyelinating lesions in the white matter are at least partially responsible for functional deficits after SCI. It has been demonstrated that newly generated oligodendrocytes are capable of remyelinating axons. Therefore, it is conceivable that the expanded pool of proliferating glial progenitor cells by F3.VEGF could induce remyelination and lead to functional recovery. We showed that F3.VEGF grafts markedly enhanced tissue sparing. NG2 glial progenitor cells stimulated by VEGF might differentiate into myelinating oligodendrocytes and enhance remyelination, eventually leading to the increase in the volume of myelinated white matter. ISC deficiency results in profound deficiencies in the mitochondrial respiratory chain complexes I, II, and III and of the Krebs cycle enzyme aconitase, all of which require ISCs for electron transfer catalysis.