• We generated new Type IIS compatible basic parts that are relevant for further investigation of human T1D
• We designed Type IIS L1 transcription units using T1D related genes and have complete gene maps for these L1 parts.
• For short sequences like the 1x and 4x uORF, it may be more efficient to synthesize these parts rather than perform PCR or digestion to obtain the fragments.
• We generated and stored plasmids and bacterial cultures from the Distribution Kit that can be shared upon request

The first section of the part collection (BBa_J435263, BBa_J433002, BBa_J433006, BBa_J433005, BBa_J433045) is designed for the enhancement of Reg3g. The Reg3g gene has been shown to reduce lymphocytic infiltration in intra-islet and peri-islet regions, indicating reduced autoimmune activity. Considering the critical role of Beta cells in insulin production for T1D patients, we have chosen to overexpress the Reg3-ʏ gene. This overexpression can facilitate leptin secretion, potentially promoting beta cell regeneration. The parts in the second section of the collection (BBa_K4748002, BBa_K4748003) are designed for the overexpressing mutated RNLS (dominant negative). RNLS is a gene expressed in the pancreas that plays a vital role in protecting beta cells from death due to ER stress and inflammation, both implicated in beta cell destruction in T1D. Mutant RNLS NIT-1 cells exhibit resistance to death induced by ER stressors like thapsigargin (TG). By overexpressing mutated RNLS (dominant negative), we can disrupt the cell line and halt the production of normal RNLS. We have removed the catalytic domain in the RNLS amino oxidase variant, rendering the protein non-functional. This modification aims to reduce the activity of autoreactive CD8+ T cells, potentially leading to fewer attacks on insulin-producing beta cells.