Western Blotting (WB), Immunohistochemistry (IHC), ELISA
纯化方法
Antigen affinity purified
免疫原
This SUMO4 antibody was produced from rabbits immunized with a KLH conjugated peptide CEPRGLS(V)KQIRFRFG selected from human SUMO4. This antibody is affinity purified using peptides CEPRGLS(V)KQIRFRFG (positive selection) and CEPRGLS(M)KQIRFRFG (negative selection).
Titration of the SUMO4 antibody may be required due to differences in protocols and secondary/substrate sensitivity.\. Western blot: 1:1000,IHC (Paraffin): 1:50-1:100
限制
仅限研究用
状态
Liquid
缓冲液
In 1X PBS, pH 7.4, with 0.09 % sodium azide
储存液
Sodium azide
注意事项
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
储存条件
-20 °C
储存方法
Aliquot the SUMO4 antibody and store frozen at -20°C or colder. Avoid repeated freeze-thaw cycles.
抗原
SUMO4
(Small Ubiquitin Related Modifier 4 (SUMO4))
IDDM5 antibody, SMT3H4 antibody, SUMO-4 antibody, dJ281H8.4 antibody, small ubiquitin-like modifier 4 antibody, small ubiquitin-related modifier 4 antibody, SMT3 suppressor of mif two 3 homolog 4 (S. cerevisiae) antibody, SUMO4 antibody, sumo4 antibody
背景
SUMO4 is a member of the SUMO gene family. This family of small ubiquitin-related modifiers covalently modify target lysines in proteins and control the target proteins' subcellular localization, stability, or activity. Upon oxidative stress, SUMO4 conjugates to various anti-oxidant enzymes, chaperones, and stress defense proteins. This protein may also conjugate to NFKBIA, TFAP2A and FOS, negatively regulating their transcriptional activity, and to NR3C1, positively regulating its transcriptional activity. Covalent attachment to SUMO4 substrates requires prior activation by the E1 complex SAE1-SAE2 and linkage to the E2 enzyme UBE2I. In contrast to SUMO1, SUMO2 and SUMO3, SUMO4 seems to be insensitive to sentrin-specific proteases due to the presence of Pro-90. This may impair processing to mature form and conjugation to substrates. SUMO4 is located in the cytoplasm and specifically modifies IKBA, leading to negative regulation of NF-kappa-B-dependent transcription of the IL12B gene. The M55V substitution has been associated with type I diabetes.