Sp100 nuclear antigen

Sp100 nuclear antigen

Protbox
Name= Sp100 nuclear antigen
Photo=
Caption=
HGNCid = 11206
Symbol = SP100
AltSymbols =
Chromosome = 2
Arm = q
Band = 37.1
LocusSupplementaryData =
Gene= SP100
Gene_type=
Protein_length=
Molecular_weight= 100k
Structure=
Type=
Functions= Normal-unknown
Domains=
Motifs=
Alternative_products=
Catalytic_activity=
Cofactors= NUPs
Enzyme_regulation=
Km=
Vmax=
Biophysicochemical_properties=
Diseases=
Pharmaceuticals=
Biotechnology=
Taxa= Homo sapiens
Cells= All
Location= Nucleoplasm, Chromatin
Mods=
Names=
Pathways=
Interactions= Autoantigenic
Actions=
Agonists=
Antagonists=
Accession_numbers= AF056322
EntrezGene = 6672
OMIM = 604585
RefSeq = NM_003113
UniProt = P23497
PDB = 1H5P
ECnumber =
Codes=
Review=
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Sp100 nuclear antigen is an interferon stimulated antigenfound in the bile duct of primary biliary cirrhosis.cite journal | author = Szostecki C, Guldner HH, Netter HJ, Will H | title = Isolation and characterization of cDNA encoding a human nuclear antigen predominantly recognized by autoantibodies from patients with primary biliary cirrhosis | journal = J. Immunol. | volume = 145 | issue = 12 | pages = 4338–47 | year = 1990 | pmid = 2258622 | doi = ] Histologically sp100 'dots' regions of the cell nucleus. Viral infection and mitogens affect the expression of the Sp100 autoantigen. Cells grown in the presence of interferons(α,β, and γ)revealed an increase both in size and number of the Sp100 protein-containing nuclear dots and increase the protein concentration. This raises "the question whether cytokine-mediated increase of Sp100 protein expression plays a role in induction of anti-Sp100 autoantibodies."cite journal |author=Guldner HH, Szostecki C, Grötzinger T, Will H |title=IFN enhance expression of Sp100, an autoantigen in primary biliary cirrhosis |journal=J. Immunol. |volume=149 |issue=12 |pages=4067–73 |year=1992 |pmid=1281200 |doi= |issn=]

p100 and Nuclear Dots

Two proteins, sp100 and Promycrocytic leukemia (PML) factor are localized to punctate domains in the nucleus (nuclear dots or nuclear bodies). These domains (few to 20) were found to form a donut shaped structure when cells were starved of amino acids. In particular, depravation of cystine results in most pronounced changes.cite journal | author = Kamei H | title = Cystine starvation induces reversible large-body formation from nuclear bodies in T24 cells | journal = Exp. Cell Res. | volume = 237 | issue = 1 | pages = 207–16 | year = 1997 | pmid = 9417884 | doi = 10.1006/excr.1997.3790] Two other proteins, PIC1/SUMO-1, that also interact with nuclear pore complex factors also interact with these two proteins.cite journal | author = Sternsdorf T, Jensen K, Will H | title = Evidence for covalent modification of the nuclear dot-associated proteins PML and Sp100 by PIC1/SUMO-1 | journal = J. Cell Biol. | volume = 139 | issue = 7 | pages = 1621–34 | year = 1997 | pmid = 9412458 | doi = ] In addition sp100 interacts with a chromatin binding protein, HM1.cite journal | author = Seeler JS, Marchio A, Sitterlin D, Transy C, Dejean A | title = Interaction of SP100 with HP1 proteins: a link between the promyelocytic leukemia-associated nuclear bodies and the chromatin compartment | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 95 | issue = 13 | pages = 7316–21 | year = 1998 | pmid = 9636146 | doi = ]

p100 Splicoforms

Some sp100 variants contain a domain similar to two interferon-inducible nuclear phosphoproteins, suppressin and DEAF-1. This defines a novel protein motif, the HNPP-box. Another class of variants has high mobility group 1 (HMG1) protein sequence as a domain. Both major classes of Sp100 splice variant proteins localize in part to nuclear dots/PML bodies and other nuclear domains. cite journal | author = Guldner HH, Szostecki C, Schröder P, "et al" | title = Splice variants of the nuclear dot-associated Sp100 protein contain homologies to HMG-1 and a human nuclear phosphoprotein-box motif | journal = J. Cell. Sci. | volume = 112 ( Pt 5) | issue = | pages = 733–47 | year = 1999 | pmid = 9973607 | doi = ]

=References=


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