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The modification of proteins with ubiquitin is an important cellular mechanism for targeting abnormal or short-lived proteins for degradation. Additionally we are shipping Ubiquitin-Conjugating Enzyme E2A Antibodies (45) and Ubiquitin-Conjugating Enzyme E2A Proteins (16) and many more products for this protein.
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Data show that the ubiquitin-conjugating enzyme E2 RAD6A/B-MDM2 ubiquitin ligase machinery regulates anti-silencing function 1A protein (ASF1A) degradation.
Results showed KCMF1 (show KCMF1 ELISA Kits) C-terminus binds directly to RAD6, whereas N-terminal domains interact with UBR4 (show UBR4 ELISA Kits) and point mutations found in X-linked intellectual disability (XLID) patients specifically lose the interaction with KCMF1 (show KCMF1 ELISA Kits) and UBR4 (show UBR4 ELISA Kits).
This study investigates clinical and molecular data of two unrelated, affected males with chromosome Xq24 deletions encompassing UBE2A.
RAD6 physically interacts with heterochromatin protein 1alpha and ubiquitinates HP1alpha (show CBX5 ELISA Kits) at residue K154, thereby promoting heterochromatin protein 1alpha degradation through the autophagy pathway
HHR6 and hRad18 (show RAD18 ELISA Kits) can monoubiquitinate FANCD2 (show FANCD2 ELISA Kits) at lysine 561 in vitro. This activity may represent a novel stress response pathway.
RNF168 (show RNF168 ELISA Kits), in complex with RAD6A or RAD6B (show UBE2B ELISA Kits), is activated in the DNA-damage-induced protein ubiquitination cascade.
RAD6A is a regulator of Parkin (show PARK2 ELISA Kits)-dependent mitophagy plays a critical role in maintaining neuronal function.
UBE2A specifically interacts with CDK9 (show CDK9 ELISA Kits), but not CDK2 (show CDK2 ELISA Kits) and is phosphorylated by CDK9 (show CDK9 ELISA Kits) in vitro.
RAD6 can form a ternary complex with MDM2 (show MDM2 ELISA Kits) and p53 (show TP53 ELISA Kits) that contributes to the degradation of p53 (show TP53 ELISA Kits).
UBE2A deficiency syndrome is reported in two male patients.
results indicate a causal role of UBE2A in learning and mGLUR (show GRM8 ELISA Kits)-dependent long-term depression
Disruption of pre-TCR expression accelerates lymphomagenesis in E2A (show TCF3 ELISA Kits)-deficient mice.
signaling through Notch (show NOTCH1 ELISA Kits) modulates the turnover of E2A (show TCF3 ELISA Kits) proteins
absence of mHR6A in oocytes prevents development beyond the embryonic two-cell stage
The modification of proteins with ubiquitin is an important cellular mechanism for targeting abnormal or short-lived proteins for degradation. Ubiquitination involves at least three classes of enzymes: ubiquitin-activating enzymes, or E1s, ubiquitin-conjugating enzymes, or E2s, and ubiquitin-protein ligases, or E3s. This gene encodes a member of the E2 ubiquitin-conjugating enzyme family. This enzyme is required for post-replicative DNA damage repair. Multiple alternatively spliced transcript variants have been found for this gene and they encode distinct isoforms.
ubiquitin-conjugating enzyme E2 A
, ubiquitin-conjugating enzyme E2A (RAD6 homolog)
, ubiquitin-conjugating enzyme E2A
, RAD6 homolog A
, ubiquitin carrier protein A
, ubiquitin-protein ligase A
, ubiquitin-conjugating enzyme E2A, RAD6 homolog
, ubiquitin-conjugating enzyme HR6A