The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
- First try to dissolve a small amount of peptide in either water or buffer. The more charged residues on a peptide, the more soluble it is in aqueous solutions. - If the peptide doesn’t dissolve try an organic solvent e.g. DMSO, then dilute using water or buffer. - Consider that any solvent used must be compatible with your assay. If a peptide does not dissolve and you need to recover it, lyophilise to remove the solvent. - Gentle warming and sonication can effectively aid peptide solubilisation. If the solution is cloudy or has gelled the peptide may be in suspension rather than solubilised. - Peptides containing cysteine are easily oxidised, so should be prepared in solution just prior to use.
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Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
Information available upon request.
GAP modifying protein 1
GAP-modifying protein 1
Small ubiquitin related modifier 1
Small ubiquitin-like modifier 1
Small ubiquitin-related modifier 1
SMT3 homolog 3
SMT3 suppressor of mif two 3 homolog 1
SMT3, yeast, homolog 3
Ubiquitin homology domain protein PIC1
Ubiquitin Like 1
Ubiquitin like protein SMT3C
Ubiquitin like protein UBL1
Ubiquitin-homology domain protein PIC1
Ubiquitin-like protein SMT3C
Ubiquitin-like protein UBL1
Ubiquitin-like protein that can be covalently attached to proteins as a monomer or a lysine-linked polymer. Covalent attachment via an isopeptide bond to its substrates requires prior activation by the E1 complex SAE1-SAE2 and linkage to the E2 enzyme UBE2I, and can be promoted by E3 ligases such as PIAS1-4, RANBP2 or CBX4. This post-translational modification on lysine residues of proteins plays a crucial role in a number of cellular processes such as nuclear transport, DNA replication and repair, mitosis and signal transduction. Involved for instance in targeting RANGAP1 to the nuclear pore complex protein RANBP2. Polymeric SUMO1 chains are also susceptible to polyubiquitination which functions as a signal for proteasomal degradation of modified proteins. May also regulate a network of genes involved in palate development.
Defects in SUMO1 are the cause of non-syndromic orofacial cleft type 10 (OFC10) [MIM:613705]; also called non-syndromic cleft lip with or without cleft palate 10. OFC10 is a birth defect consisting of cleft lips with or without cleft palate. Cleft lips are associated with cleft palate in two-third of cases. A cleft lip can occur on one or both sides and range in severity from a simple notch in the upper lip to a complete opening in the lip extending into the floor of the nostril and involving the upper gum. Note=A chromosomal aberation involving SUMO1 is the cause of OFC10. Translocation t(2;8)(q33.1;q24.3). The breakpoint occurred in the SUMO1 gene and resulted in haploinsufficiency confirmed by protein assays.
Belongs to the ubiquitin family. SUMO subfamily. Contains 1 ubiquitin-like domain.
Cleavage of precursor form by SENP1 or SENP2 is necessary for function. Polymeric SUMO1 chains undergo polyubiquitination by RNF4.
Nucleus membrane. Nucleus speckle. Cytoplasm. Recruited by BCL11A into the nuclear body.