Prolifeing Cell Nuclear Antigen
Recombinant ID:
2664
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Gene of Interest
Gene Synonyms:
Protein Names:
Accession Data
Organism:
Homo sapiens (Human)
Mass (kDa):
28769
Length (aa):
261
Sequence:
MFEARLVQGSILKKVLEALKDLINEACWDISSSGVNLQSMDSSHVSLVQLTLRSEGFDTYRCDRNLAMGVNLTSMSKILKCAGNEDIITLRAEDNADTLALVFEAPNQEKVSDYEMKLMDLDVEQLGIPEQEYSCVVKMPSGEFARICRDLSHIGDAVVISCAKDGVKFSASGELGNGNIKLSQTSNVDKEEEAVTIEMNEPVQLTFALRYLNFFTKATPLSSTVTLSMSADVPLVVEYKIADMGHLKYYLAPKIEDEEGS
Proteomics (Proteome ID):
Proliferating cell nuclear antigen (PCNA) (Cyclin)
Proteomics (Chromosome):
UP000005640
Mass Spectrometry:
N/A
Function [CC]:
Auxiliary protein of DNA polymerase delta and is involved in the control of eukaryotic DNA replication by increasing the polymerase's processibility during elongation of the leading strand. Induces a robust stimulatory effect on the 3'-5' exonuclease and 3'-phosphodiesterase, but not apurinic-apyrimidinic (AP) endonuclease, APEX2 activities. Has to be loaded onto DNA in order to be able to stimulate APEX2. Plays a key role in DNA damage response (DDR) by being conveniently positioned at the replication fork to coordinate DNA replication with DNA repair and DNA damage tolerance pathways (PubMed:24939902). Acts as a loading platform to recruit DDR proteins that allow completion of DNA replication after DNA damage and promote postreplication repair: Monoubiquitinated PCNA leads to recruitment of translesion (TLS) polymerases, while 'Lys-63'-linked polyubiquitination of PCNA is involved in error-free pathway and employs recombination mechanisms to synthesize across the lesion (PubMed:24695737). {ECO:0000269|PubMed:18719106, ECO:0000269|PubMed:19443450, ECO:0000269|PubMed:24695737, ECO:0000269|PubMed:24939902}.
Metal Binding:
N/A
Site:
N/A
Tissue Specificity:
N/A
Disease:
Ataxia-telangiectasia-like disorder 2 (ATLD2) [MIM:615919]: A neurodegenerative disorder due to defects in DNA excision repair. ATLD2 is characterized by developmental delay, ataxia, sensorineural hearing loss, short stature, cutaneous and ocular telangiectasia, and photosensitivity. {ECO:0000269|PubMed:24911150}. Note=The disease is caused by mutations affecting the gene represented in this entry.
Mutagenesis:
MUTAGEN 13 13 K->R: Inhibits acetylation, recruitment to DNA damage sites, inducible ubiquitination and protein degradation, DNA replication and repair synthesis efficiencies, but homotrimer formation, nuclear recruitment to DNA damage sites, interactions with CREBBP, EP300 and POLD1 are similar as the wild-type; in association with R-14; R-20; R-77 and R-80. {ECO:0000269|PubMed:24939902}.; MUTAGEN 14 14 K->R: Inhibits acetylation, recruitment to DNA damage sites, inducible ubiquitination and protein degradation, DNA replication and repair synthesis efficiencies, but homotrimer formation, nuclear recruitment to DNA damage sites, interactions with CREBBP, EP300 and POLD1 are similar as the wild-type; in association with R-13; R-20; R-77 and R-80. {ECO:0000269|PubMed:24939902}.; MUTAGEN 20 20 K->R: Inhibits acetylation, recruitment to DNA damage sites, inducible ubiquitination and protein degradation, DNA replication and repair synthesis efficiencies, but homotrimer formation, nuclear recruitment to DNA damage sites, interactions with CREBBP, EP300 and POLD1 are similar as the wild-type; in association with R-13; R-14; R-77 and R-80. {ECO:0000269|PubMed:24939902}.; MUTAGEN 43 45 SHV->AAA: No effect on POLD3-binding. {ECO:0000269|PubMed:11595739}.; MUTAGEN 77 77 K->A: Inhibits recruitment to DNA damage sites, but nuclear localization is similar as the wild-type; in association with A-80. {ECO:0000269|PubMed:24939902}.; MUTAGEN 77 77 K->R: Inhibits acetylation, recruitment to DNA damage sites, inducible ubiquitination and protein degradation, DNA replication and repair synthesis efficiencies, but homotrimer formation, nuclear recruitment to DNA damage sites, interactions with CREBBP, EP300 and POLD1 are similar as the wild-type; in association with R-13; R-14; R-20 and R-80. {ECO:0000269|PubMed:24939902}.; MUTAGEN 80 80 K->A: Inhibits recruitment to DNA damage sites, but nuclear localization is similar as the wild-type; in association with A-77. {ECO:0000269|PubMed:24939902}.; MUTAGEN 80 80 K->R: Inhibits acetylation, recruitment to DNA damage sites, inducible ubiquitination and protein degradation, DNA replication and repair synthesis efficiencies, but homotrimer formation, nuclear recruitment to DNA damage sites, interactions with CREBBP, EP300 and POLD1 are similar as the wild-type; in association with R-13; R-14; R-20 and R-77. {ECO:0000269|PubMed:24939902}.; MUTAGEN 125 128 QLGI->AAAA: Strong decrease in POLD3-binding. {ECO:0000269|PubMed:11595739}.; MUTAGEN 164 164 K->R: Abolishes ubiquitination. No effect on interaction with SHPRH. {ECO:0000269|PubMed:17108083, ECO:0000269|PubMed:17130289, ECO:0000269|PubMed:18719106, ECO:0000269|PubMed:20129063}.; MUTAGEN 188 190 VDK->AAA: No effect on POLD3-binding. {ECO:0000269|PubMed:11595739}.; MUTAGEN 211 211 Y->F: Alters chromatin-associated PCNA stability and its function in DNA replication and repair. {ECO:0000269|PubMed:17115032}.; MUTAGEN 251 254 LAPK->AAAA: Decrease in POLD3-binding. {ECO:0000269|PubMed:11595739}.
Reagent Data
Name:
Proliferating cell nuclear antigen (PCNA) (Cyclin)
Class:
Subcategory:
Recombinant
Molecular Weight:
Source:
Species:
Human
Amino Acid Sequence:
Tag:
Format:
Solution
Formulation:
Sterile-filtered colorless solution
Formulation Concentration:
1mg/ml
Buffer Volume:
20mM
Buffer Solution:
Tris
pH:
7.5
Stabilizers
NaCl:
Null
Metal Chelating Agents
EDTA:
2mM
Purity:
> 95%
Determined:
SDS-PAGE
Stained:
Inquire
Validated:
Inquire
Sample Handling
Storage:
4°C
Stability:
This bioreagent is stable at 4°C (short-term) and -70°C(long-term). After reconstitution, sample may be stored at 4°C for 2-7 days and below -18°C for future use.
Preparation:
Reconstitute in sterile distilled H2O to no less than 100ug/ml; dilute reconstituted stock further in other aqueous solutions if needed. Please review COA for lot-specific instructions. Final measurements should be determined by the end-user for optimal performance.