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Tripartite motif containing 22

TRIM22, Staf50, tripartite motif-containing 22, stimulated trans-acting factor
The protein encoded by this gene is a member of the tripartite motif (TRIM) family. The TRIM motif includes three zinc-binding domains, a RING, a B-box type 1 and a B-box type 2, and a coiled-coil region. This protein localizes to the cytoplasm and its expression is induced by interferon. The protein down-regulates transcription from the HIV-1 LTR promoter region, suggesting that function of this protein may be to mediate interferon's antiviral effects. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Dec 2010] (from NCBI)
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Top mentioned proteins: Trim, TRIM5alpha, p53, HAD, ACID
Papers on TRIM22
Interferon alpha (IFNα)-induced TRIM22 interrupts HCV replication by ubiquitinating NS5A.
Sun et al., Shanghai, China. In Cell Mol Immunol, Jan 2016
TRIM22, a tripartite-motif (TRIM) protein, is upregulated upon interferon alpha (IFNα) administration to hepatitis C virus (HCV)-infected patients.
APOE*E2 allele delays age of onset in PSEN1 E280A Alzheimer's disease.
Arcos-Burgos et al., Canberra, Australia. In Mol Psychiatry, Jan 2016
Exploratory linear mixed-effects multilocus analysis suggested that other functional variants harbored in genes involved in cell proliferation, protein degradation, apoptotic and immune dysregulation processes (i.e., GPR20, TRIM22, FCRL5, AOAH, PINLYP, IFI16, RC3H1 and DFNA5) might interact with the APOE*E2 allele.
Short-term Treatment With Interferon Alfa Diminishes Expression of HIV-1 and Reduces CD4+ T-Cell Activation in Patients Coinfected With HIV and Hepatitis C Virus and Receiving Antiretroviral Therapy.
Martinez-Picado et al., Vic, Spain. In J Infect Dis, Dec 2015
No changes were detected in levels of residual plasma viremia, replication-competent reservoirs, proviral DNA, or 2-long-terminal repeat circles, although APOBEC3G, TRIM5α, BST2, and TRIM22 were upregulated in the IFN group.
Increased expression and dysregulated association of restriction factors and type I interferon in HIV, HCV mono- and co-infected patients.
Zheng et al., Kunming, China. In J Med Virol, Dec 2015
In this study, we measured the levels of TRIM5α, TRIM22, APOBEC3G, and IFN-α, -β mRNA expression in peripheral blood mononuclear cells of 43 HIV mono-infected, 70 HCV mono-infected and 64 HIV/HCV co-infected patients along with 98 healthy controls.
Control of FoxO4 Activity and Cell Survival by TRIM22 Directs TLR3-Stimulated Cells Toward IFN Type I Gene Induction or Apoptosis.
Mechti et al., Montpellier, France. In J Interferon Cytokine Res, Nov 2015
In addition, we show that the IFN-induced TRIM22 ubiquitin ligase targets FoxO4 and antagonizes its activity through an unrelated ubiquitin/autophagosomic-lysosomal pathway.
Identification of TRIM22 as a progesterone-responsive gene in Ishikawa endometrial cancer cells.
Inoue et al., Tokyo, Japan. In J Steroid Biochem Mol Biol, Nov 2015
Out of these 15 genes, we focused on TRIM22.
Single nucleotide polymorphisms/haplotypes associated with multiple rubella-specific immune response outcomes post-MMR immunization in healthy children.
Poland et al., Rochester, United States. In Immunogenetics, Oct 2015
Of these SNPs, we detected eight in the PVRL3 gene, five in the PVRL1 gene, one in the TRIM22 gene, two in the IL10RB gene, two in the TLR4 gene, and five in other genes (PVR, ADAR, ZFP57, MX1, and BTN2A1/BTN3A3).
Reduced Simian Immunodeficiency Virus Replication in Macrophages of Sooty Mangabeys Is Associated with Increased Expression of Host Restriction Factors.
Silvestri et al., Atlanta, United States. In J Virol, Oct 2015
Interestingly, we found that SM macrophages exhibited a significantly greater increase in the expression of tetherin (P = 0.003) and TRIM22 (P = 0.0006) in response to alpha interferon stimulation and increased expression of multiple host restriction factors in response to lipopolysaccharide stimulation and exposure to SIV.
Antiviral gene expression in psoriasis.
Liao et al., San Francisco, United States. In J Eur Acad Dermatol Venereol, Oct 2015
RESULTS: We observed significant overexpression of 16 antiviral genes in lesional psoriatic skin, with a greater than two-fold increase in ISG15, RSAD2, IRF7, MX2 and TRIM22 (P < 1E-07).
[Expressions and co-localization of HIV capsid protein p24 and TRIM22 in HEK293T cells].
Xu et al., Yantai, China. In Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi, Aug 2015
OBJECTIVE: To observe the co-localization of human immunodeficiency virus (HIV) capsid protein p24 and tripartite motif containing 22 (TRIM22) in HEK293T cells.
TRIM22 can activate the noncanonical NF-κB pathway by affecting IKKα.
Yang et al., Wuhan, China. In J Recept Signal Transduct Res, 2014
Tripartite motif 22 (TRIM22) is involved in various cellular processes.
HIV-1 transcriptional silencing caused by TRIM22 inhibition of Sp1 binding to the viral promoter.
Vicenzi et al., Milano, Italy. In Retrovirology, 2014
Among these, we have shown that Tripartite motif 22 (TRIM22) suppresses basal as well as phorbol ester-induced HIV-1 long terminal repeat (LTR)-mediated transcription, independently of its E3 ubiquitin ligase activity, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) binding to the U3 region and Tat interaction with the TAR region of the HIV-1 LTR.
TRIM59 Promotes the Proliferation and Migration of Non-Small Cell Lung Cancer Cells by Upregulating Cell Cycle Related Proteins.
Wang et al., Nanchang, China. In Plos One, 2014
In an effort to profile the expression patterns of TRIM superfamily in several non-small cell lung cancer (NSCLC) cell lines, we found that the expression of 10 TRIM genes including TRIM3, TRIM7, TRIM14, TRIM16, TRIM21, TRIM22, TRIM29, TRIM59, TRIM66 and TRIM70 was significantly upregulated in NSCLC cell lines compared with the normal human bronchial epithelial (HBE) cell line, whereas the expression of 7 other TRIM genes including TRIM4, TRIM9, TRIM36, TRIM46, TRIM54, TRIM67 and TRIM76 was significantly down-regulated in NSCLC cell lines compared with that in HBE cells.
Restriction Factors in HIV-1 Disease Progression.
Berthoux et al., Trois-Rivières, Canada. In Curr Hiv Res, 2014
TRIM5α, Mx2/MxB, TRIM22/Staf50, SAMHD1, p21/CDKN1, tetherin/BST2/CD137, APOBEC3G and APOBEC3F have all been proposed to inhibit HIV-1, often with gene variant- or cellular context-specificity.
BRG1 is indispensable for IFN-γ-induced TRIM22 expression, which is dependent on the recruitment of IRF-1.
Xiong et al., Shanghai, China. In Biochem Biophys Res Commun, 2011
BRG1-mediated chromatin remodeling is critical for the IFN-gamma-inducibility of TRIM22 gene.
Identification of tripartite motif-containing 22 (TRIM22) as a novel NF-κB activator.
Xiong et al., Shanghai, China. In Biochem Biophys Res Commun, 2011
These data suggested that TRIM22 was a positive regulator of NF-kappaB-mediated transcription.
TRIM22 inhibits HIV-1 transcription independently of its E3 ubiquitin ligase activity, Tat, and NF-kappaB-responsive long terminal repeat elements.
Vicenzi et al., Milano, Italy. In J Virol, 2011
Nuclear TRIM22 significantly impairs HIV-1 replication, likely by interfering with Tat- and NF-kappaB-independent long-terminal-repeat-driven transcription.
Association of TRIM22 with the type 1 interferon response and viral control during primary HIV-1 infection.
CAPRISA Acute Infection Study Team et al., Durban, South Africa. In J Virol, 2011
These data suggest concordance between type 1 IFN and TRIM22 in PBMCs and that TRIM22 likely acts as an antiviral effector in HIV-1 infection.
Restriction factors of retroviral replication: the example of Tripartite Motif (TRIM) protein 5 alpha and 22.
Vicenzi et al., Milano, Italy. In Amino Acids, 2010
REVIEW: current knowledge on the anti-retroviral effects of TRIM5 alpha and TRIM22
The human IFN-inducible p53 target gene TRIM22 colocalizes with the centrosome independently of cell cycle phase.
Drott et al., Lund, Sweden. In Exp Cell Res, 2010
endogenous TRIM22 is localized to both nucleus and cytosol in primary human mononuclear cells, as well as in the human osteosarcoma cell line U2OS
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