2.3.2.23: E2 ubiquitin-conjugating enzyme
This is an abbreviated version!
For detailed information about E2 ubiquitin-conjugating enzyme, go to the full flat file.
Word Map on EC 2.3.2.23
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2.3.2.23
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proteasome
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ligases
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polyubiquitination
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sumoylation
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ubiquitin-like
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finger
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ubiquitin-proteasome
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ubiquitylation
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monoubiquitination
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ubiquitin-protein
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ubiquitin-activating
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k63-linked
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ubiquitin-dependent
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cullins
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parkin
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ubiquitin-mediated
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ubiquitin-related
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fanconi
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anaphase-promoting
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deubiquitinating
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cullin-ring
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isopeptide
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error-free
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isg15
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lys63-linked
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neddylation
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cdc20
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sumo1
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autoubiquitination
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traf6
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er-associated
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ring-h2
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ranbp2
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tak1
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thiolester
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ring-finger
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sic1
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e3-ligase
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multiubiquitination
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tpx2
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rbx1
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translesion
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fancd2
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aurka
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postreplication
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conjugase
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ubiquitin-binding
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ubiquitin-ligase
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ring-type
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medicine
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nonerythroid
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diagnostics
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drug development
- 2.3.2.23
- proteasome
- ligases
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polyubiquitination
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sumoylation
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ubiquitin-like
- finger
-
ubiquitin-proteasome
-
ubiquitylation
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monoubiquitination
- ubiquitin-protein
-
ubiquitin-activating
-
k63-linked
-
ubiquitin-dependent
-
cullins
- parkin
-
ubiquitin-mediated
-
ubiquitin-related
-
fanconi
-
anaphase-promoting
-
deubiquitinating
-
cullin-ring
-
isopeptide
-
error-free
- isg15
-
lys63-linked
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neddylation
- cdc20
- sumo1
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autoubiquitination
- traf6
-
er-associated
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ring-h2
- ranbp2
- tak1
- thiolester
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ring-finger
- sic1
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e3-ligase
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multiubiquitination
- tpx2
- rbx1
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translesion
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fancd2
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aurka
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postreplication
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conjugase
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ubiquitin-binding
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ubiquitin-ligase
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ring-type
- medicine
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nonerythroid
- diagnostics
- drug development
Reaction
Synonyms
alpha spectrin, ARIH1, At1g78870, At2g02760, CDC34, Cdc34B, Ci0100152677, E2 enzyme, E2 Ub-conjugating enzyme, E2 ubiquitin conjugating enzyme, E2 ubiquitin-conjugating enzyme, E2-20K, E2-25K, E2-conjugating enzyme, E2-ubiquitin conjugating enzyme, FANCT, HOYS7, Mms2, NCUBE1, NEDD8-activating enzyme E1 catalytic subunit, Pex4, Rad6a, RAD6B, Rad6p, SCEI, SUMO E2 conjugating enzyme, SUMO E2 enzyme, SUMO-1-conjugating enzyme Ubc9, SUMO-conjugating enzyme UBC9, UBA2, Uba3, UBA6-specific E2 enzyme 1, UBC E2, Ubc-18, Ubc1, Ubc11, Ubc13, Ubc2, Ubc35, Ubc3B, Ubc4, Ubc4/5, Ubc5a, Ubc6, UBC6e, UBC7, Ubc8, Ubc9, UbcA1, UBCE4, UbcH10, UBCH2, UbcH3, UbcH5A, UbcH5B, UbcH5C, UbcH5D, UbcH6, UbcH7, UbcH8, UbcH9, UbcM2, UbcM4, Ube2, UBE2A, UBE2B, UBE2C, UBE2D, UBE2D1, ube2d1b, UBE2D2, UBE2D3, UBE2D4, UBE2E1, UBE2E2, UBE2E3, Ube2G, UBE2G1, UBE2G2, UBE2H, Ube2I, Ube2J1, UBE2J2, UBE2K, UBE2L3, UBE2L6, UBE2N, Ube2NL, UBE2Q1, UBE2Q2, UBE2QL, UBE2QL1, Ube2r, UBE2R1, UBE2R2, UBE2S, UBE2T, UBE2U, Ube2V, UBE2V1, UBE2V2, UBE2W, UBE2Z, ubiquitin-conjugating enzyme, ubiquitin-conjugating enzyme (E2), ubiquitin-conjugating enzyme E2, ubiquitin-conjugating enzyme E2 B, ubiquitin-conjugating enzyme E2 D1, ubiquitin-conjugating enzyme E2 G1, ubiquitin-conjugating enzyme E2 Z, ubiquitin-conjugating enzyme E2-20 kDa, ubiquitin-conjugating enzyme E2T, ubiquitination enzyme, Uev1, Uev1A, Uev2, USE1, VvUBC
ECTree
2.3.2.23 E2 ubiquitin-conjugating enzymeAdvanced search results
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results (Engineering
Engineering on EC 2.3.2.23 - E2 ubiquitin-conjugating enzyme
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
A157C
a naturally occuring mutation involved in the Fanconi anaemia syndrome
C136F
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mutation results in constitutive binding of UbcM2 to transcription factor Nrf2 and an increased half-life of the transcription factor in vivo
C94S
site-directed mutagenesis, a catalytically inactive mutant
D102K
site-directed mutagenesis, analysis of ubiquitin specificity and reaction kinetics compared to wild-type
D103K
site-directed mutagenesis, analysis of ubiquitin specificity and reaction kinetics compared to wild-type
D143A
site-directed mutagenesis, analysis of ubiquitin specificity and reaction kinetics compared to wild-type
D143K
site-directed mutagenesis, analysis of ubiquitin specificity and reaction kinetics compared to wild-type
D143R
site-directed mutagenesis, analysis of ubiquitin specificity and reaction kinetics compared to wild-type
D91K
site-directed mutagenesis, analysis of ubiquitin specificity and reaction kinetics compared to wild-type
DELTA946
truncation of the Uba3 carboxyl-terminal beta-grasp domain, no effect on cognate Ubc12 thiolester formation
K323R
mutation in site of auto-FAT10ylation. Mutation does not abolish auto-FAT10ylation of USE1, but every other lysine can instead be modified with FAT10
K86V
during transfer of ubiquitin to the final substrate or E3 ligase, reaction of EC 2.3.2.27, mutant shows increased polyubiquitin chain building activity with ubiquitin mutant K48R
N80Q
during transfer of ubiquitin to the final substrate or E3 ligase, reaction of EC 2.3.2.27, mutant shows increased polyubiquitin chain building activity with ubiquitin mutant K48R
P79A
during transfer of ubiquitin to the final substrate or E3 ligase, reaction of EC 2.3.2.27, mutant shows a much reduced capacity to ubiquitylate RING-E3 enzyme RNF25
Q2E
a naturally occuring mutation involved in the Fanconi anaemia syndrome
Q37R
a naturally occuring mutation involved in the Fanconi anaemia syndrome
R13A/K14A
mutations in Ubc9 disrupt the interaction with SUMO-1 but do not completely abolish the interaction with E1 enzyme. Mutant displays a significantly reduced efficiency in the transfer of SUMO-1 from E1 to Ubc9, its ability to recognize substrate and transfer SUMO-1 from Ubc9 to the target protein is unaffected
R17A/K18A
mutations in Ubc9 disrupt the interaction with SUMO-1 but do not completely abolish the interaction with E1 enzyme. Mutant displays a significantly reduced efficiency in the transfer of SUMO-1 from E1 to Ubc9, its ability to recognize substrate and transfer SUMO-1 from Ubc9 to the target protein is unaffected
R94Q/L98M
during transfer of ubiquitin to the final substrate or E3 ligase, reaction of EC 2.3.2.27, mutant shows increased polyubiquitin chain building activity with ubiquitin mutant K48R
C105S/C146S
mutation of the residues forming an intramolecular disulfide bond. Mutation does not disturb the secondary structure of the protein but does reduce the in vitro activity of isoform Pex4
K118R
residue Lys118 is required for Ubc7 activity. Mutant is very poor in assembly of polyubiquitin chains. Lys118 is both essential and sufficient for Doa10-mediated degradation of substrates
P93L
additional information
P93L
temperature-sensitive mutant in which cell cycle progression is arrested at mitosis. The mutant grows normally at the restrictive temperature when spindle assembly checkpoint is inactivated, suggesting that the arrest is not due to abnormal spindle assembly, but rather due to prolonged activation of spindle assembly checkpoint
P93L
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temperature-sensitive mutant in which cell cycle progression is arrested at mitosis. The mutant grows normally at the restrictive temperature when spindle assembly checkpoint is inactivated, suggesting that the arrest is not due to abnormal spindle assembly, but rather due to prolonged activation of spindle assembly checkpoint
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additional information
DNA damage-induced foci of E2 ubiquitin-conjugating enzyme are detectable upon co-transfection with an interacting E3 ubiquitin ligase
additional information
DNA damage-induced foci of E2 ubiquitin-conjugating enzyme are detectable upon co-transfection with an interacting E3 ubiquitin ligase
additional information
enzyme knockout by UBE2J2 siRNA in Hep-G2 cells. HEK293T cells lacking the E2 ubiquitin-conjugating enzymes UBE2J1, UBE2J2, and UBE2G2 are generated using a limited CRISPR/Cas9-based library. Hap1 cells lacking UBE2J2 are generated by CRISPR/Cas9-mediated genome editing
additional information
enzyme knockout by UBE2J2 siRNA in Hep-G2 cells. HEK293T cells lacking the E2 ubiquitin-conjugating enzymes UBE2J1, UBE2J2, and UBE2G2 are generated using a limited CRISPR/Cas9-based library. Hap1 cells lacking UBE2J2 are generated by CRISPR/Cas9-mediated genome editing
additional information
enzyme knockout by UBE2J2 siRNA in Hep-G2 cells. HEK293T cells lacking the E2 ubiquitin-conjugating enzymes UBE2J1, UBE2J2, and UBE2G2 are generated using a limited CRISPR/Cas9-based library. Hap1 cells lacking UBE2J2 are generated by CRISPR/Cas9-mediated genome editing
additional information
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enzyme knockout by UBE2J2 siRNA in Hep-G2 cells. HEK293T cells lacking the E2 ubiquitin-conjugating enzymes UBE2J1, UBE2J2, and UBE2G2 are generated using a limited CRISPR/Cas9-based library. Hap1 cells lacking UBE2J2 are generated by CRISPR/Cas9-mediated genome editing
additional information
enzyme UBE2B knockout, HONE-1 and TW01 cells are transfected specific UBE2B siRNA
additional information
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enzyme UBE2B knockout, HONE-1 and TW01 cells are transfected specific UBE2B siRNA
additional information
generation of deletion mutants UBE2ZDELTALB and UBE2ZDELTANter
additional information
genome analysis for patient PNGS-252 revealed a maternal c.4C>G missense alteration resulting in the Gln2Glu amino acid substitution and a paternal 23 kb deletion across the UBE2T locus. The Gln2 residue in helix1 of UBE2T is not an integral part of the UBE2T-FANCL interaction surface
additional information
genome analysis for patient PNGS-252 revealed a maternal c.4C>G missense alteration resulting in the Gln2Glu amino acid substitution and a paternal 23 kb deletion across the UBE2T locus. The Gln2 residue in helix1 of UBE2T is not an integral part of the UBE2T-FANCL interaction surface
additional information
HEK293T cells lacking the E2 ubiquitin-conjugating enzymes UBE2J1, UBE2J2 and UBE2G2 are generated using a limited CRISPR/Cas9-based library
additional information
HEK293T cells lacking the E2 ubiquitin-conjugating enzymes UBE2J1, UBE2J2 and UBE2G2 are generated using a limited CRISPR/Cas9-based library
additional information
HEK293T cells lacking the E2 ubiquitin-conjugating enzymes UBE2J1, UBE2J2 and UBE2G2 are generated using a limited CRISPR/Cas9-based library
additional information
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HEK293T cells lacking the E2 ubiquitin-conjugating enzymes UBE2J1, UBE2J2 and UBE2G2 are generated using a limited CRISPR/Cas9-based library
additional information
HEK293T cells lacking the E2 ubiquitin-conjugating enzymes UBE2J1, UBE2J2, and UBE2G2 are generated using a limited CRISPR/Cas9-based library
additional information
HEK293T cells lacking the E2 ubiquitin-conjugating enzymes UBE2J1, UBE2J2, and UBE2G2 are generated using a limited CRISPR/Cas9-based library
additional information
HEK293T cells lacking the E2 ubiquitin-conjugating enzymes UBE2J1, UBE2J2, and UBE2G2 are generated using a limited CRISPR/Cas9-based library
additional information
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HEK293T cells lacking the E2 ubiquitin-conjugating enzymes UBE2J1, UBE2J2, and UBE2G2 are generated using a limited CRISPR/Cas9-based library
additional information
knockdown of enzyme UBE2T by specific siRNA in BGC-823 cells and HTB-103 cells can induce G1/S phase arrest in gastric cancer cells, which in turn contributes to the stimulating growth properties of gastric cancer cells. Overexpression of UBE2T in AGS cells and CRL-5974 cells. Phenotypes, overview
additional information
lentiviral CRISPR/Cas9 library targeting of all known human E2 enzymes is used to assess their involvement in US2-mediated HLA-I downregulation. CRISPR gRNAs targeting UBE2D3 induce rescue of eGFP-HLA-A2 expression in US2-expressing cell. The anti-UBE2D3 gRNAs also increase the levels of endogenous HLA-A3 in these US2-expressing cells
additional information
lentiviral CRISPR/Cas9 library targeting of all known human E2 enzymes is used to assess their involvement in US2-mediated HLA-I downregulation. CRISPR gRNAs targeting UBE2D3 induce rescue of eGFP-HLA-A2 expression in US2-expressing cell. The anti-UBE2D3 gRNAs also increase the levels of endogenous HLA-A3 in these US2-expressing cells
additional information
lentiviral CRISPR/Cas9 library targeting of all known human E2 enzymes is used to assess their involvement in US2-mediated HLA-I downregulation. CRISPR gRNAs targeting UBE2D3 induce rescue of eGFP-HLA-A2 expression in US2-expressing cell. The anti-UBE2D3 gRNAs also increase the levels of endogenous HLA-A3 in these US2-expressing cells
additional information
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lentiviral CRISPR/Cas9 library targeting of all known human E2 enzymes is used to assess their involvement in US2-mediated HLA-I downregulation. CRISPR gRNAs targeting UBE2D3 induce rescue of eGFP-HLA-A2 expression in US2-expressing cell. The anti-UBE2D3 gRNAs also increase the levels of endogenous HLA-A3 in these US2-expressing cells
additional information
lentiviral CRISPR/Cas9 library targeting of all known human E2 enzymes is used to assess their involvement in US2-mediated HLA-I downregulation. Generation of a UBE2G2-null cell line. CRISPR gRNAs targeting UBE2G2 induce rescue of eGFP-HLA-A2 expression in US2-expressing cell. Expression of gRNAs targeting UBE2G2 induce the strongest rescue of eGFP-HLA-A2. The anti-UBE2G2 gRNAs also increase the levels of endogenous HLA-A3 in these US2-expressing cells. By contrast, targeting the UBE2G2 homologue UBE2G1 with CRISPR gRNAs does not affect eGFP-HLA-A2 expressions. Removal of UBE2G2 in causes a growth defect, but is not lethal. HLA-I levels are increased in UBE2G2-null cells compared to control cells, and US2 protein levels are increased, likely due to the stabilization of the US2 ERAD complex in the absence of UBE2G2
additional information
lentiviral CRISPR/Cas9 library targeting of all known human E2 enzymes is used to assess their involvement in US2-mediated HLA-I downregulation. Generation of a UBE2G2-null cell line. CRISPR gRNAs targeting UBE2G2 induce rescue of eGFP-HLA-A2 expression in US2-expressing cell. Expression of gRNAs targeting UBE2G2 induce the strongest rescue of eGFP-HLA-A2. The anti-UBE2G2 gRNAs also increase the levels of endogenous HLA-A3 in these US2-expressing cells. By contrast, targeting the UBE2G2 homologue UBE2G1 with CRISPR gRNAs does not affect eGFP-HLA-A2 expressions. Removal of UBE2G2 in causes a growth defect, but is not lethal. HLA-I levels are increased in UBE2G2-null cells compared to control cells, and US2 protein levels are increased, likely due to the stabilization of the US2 ERAD complex in the absence of UBE2G2
additional information
lentiviral CRISPR/Cas9 library targeting of all known human E2 enzymes is used to assess their involvement in US2-mediated HLA-I downregulation. Generation of a UBE2G2-null cell line. CRISPR gRNAs targeting UBE2G2 induce rescue of eGFP-HLA-A2 expression in US2-expressing cell. Expression of gRNAs targeting UBE2G2 induce the strongest rescue of eGFP-HLA-A2. The anti-UBE2G2 gRNAs also increase the levels of endogenous HLA-A3 in these US2-expressing cells. By contrast, targeting the UBE2G2 homologue UBE2G1 with CRISPR gRNAs does not affect eGFP-HLA-A2 expressions. Removal of UBE2G2 in causes a growth defect, but is not lethal. HLA-I levels are increased in UBE2G2-null cells compared to control cells, and US2 protein levels are increased, likely due to the stabilization of the US2 ERAD complex in the absence of UBE2G2
additional information
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lentiviral CRISPR/Cas9 library targeting of all known human E2 enzymes is used to assess their involvement in US2-mediated HLA-I downregulation. Generation of a UBE2G2-null cell line. CRISPR gRNAs targeting UBE2G2 induce rescue of eGFP-HLA-A2 expression in US2-expressing cell. Expression of gRNAs targeting UBE2G2 induce the strongest rescue of eGFP-HLA-A2. The anti-UBE2G2 gRNAs also increase the levels of endogenous HLA-A3 in these US2-expressing cells. By contrast, targeting the UBE2G2 homologue UBE2G1 with CRISPR gRNAs does not affect eGFP-HLA-A2 expressions. Removal of UBE2G2 in causes a growth defect, but is not lethal. HLA-I levels are increased in UBE2G2-null cells compared to control cells, and US2 protein levels are increased, likely due to the stabilization of the US2 ERAD complex in the absence of UBE2G2
additional information
lentiviral CRISPR/Cas9 library targeting of all known human E2 enzymes is used to assess their involvement in US2-mediated HLA-I downregulation. Generation of a UBE2J2-null cell line. The strong increase inHLA-I degradation upon UBE2J2 knockout is not caused by increased US2 levels. UBE2J2 depletion increases TRC8 expression levels in the presence of US2, and in this way, enhances US2-mediated HLA-I downregulation
additional information
lentiviral CRISPR/Cas9 library targeting of all known human E2 enzymes is used to assess their involvement in US2-mediated HLA-I downregulation. Generation of a UBE2J2-null cell line. The strong increase inHLA-I degradation upon UBE2J2 knockout is not caused by increased US2 levels. UBE2J2 depletion increases TRC8 expression levels in the presence of US2, and in this way, enhances US2-mediated HLA-I downregulation
additional information
lentiviral CRISPR/Cas9 library targeting of all known human E2 enzymes is used to assess their involvement in US2-mediated HLA-I downregulation. Generation of a UBE2J2-null cell line. The strong increase inHLA-I degradation upon UBE2J2 knockout is not caused by increased US2 levels. UBE2J2 depletion increases TRC8 expression levels in the presence of US2, and in this way, enhances US2-mediated HLA-I downregulation
additional information
-
lentiviral CRISPR/Cas9 library targeting of all known human E2 enzymes is used to assess their involvement in US2-mediated HLA-I downregulation. Generation of a UBE2J2-null cell line. The strong increase inHLA-I degradation upon UBE2J2 knockout is not caused by increased US2 levels. UBE2J2 depletion increases TRC8 expression levels in the presence of US2, and in this way, enhances US2-mediated HLA-I downregulation
additional information
molecular dynamics simulations for E2-25K and the Q126L/D127G active site gate mutants
additional information
Ube2D1 enzyme knockdown by specific shRNA. Treatment of HeLa cells with Ube2D1 shRNA results in a over 90% reduction in Ube2D1 protein and a 3fold increase in March-I expression, as determined by quantitative immunoblot analysis. The increase in March-I protein expression in Ube2D1 knockdown cells is correlated precisely with reduced ubiquitination of March-I
additional information
generation of UbeC6 deletion mice, phenotype, detailed overview. Generation of Derlin2-/- mice showing that not only ERAD enhancers but also UBC6e itself are upregulated
additional information
generation of a Cdc34 active site Cys to Lys mutant
additional information
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generation of a Cdc34 active site Cys to Lys mutant
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