PSMC2 (proteasome 26S subunit, ATPase 2)
- symbol:
- PSMC2
- locus group:
- protein-coding gene
- location:
- 7q22.1
- gene_family:
- AAA ATPases (ATPases associated with diverse cellular activities)|Proteasome (prosome, macropain) subunits
- alias symbol:
- MSS1|S7|Nbla10058|RPT1
- alias name:
- proteasome 26S subunit, ATPase, 2|…
- entrez id:
- 5701
- ensembl gene id:
- ENSG00000161057
- ucsc gene id:
- uc003vbs.4
- refseq accession:
- NM_002803
- hgnc_id:
- HGNC:9548
- approved reserved:
- 1995-12-22
PSMC2（Proteasome 26S Subunit, ATPase 2）是26S蛋白酶体的一个重要组成部分，属于PSMC基因家族，该家族共有6个成员（PSMC1-6），它们共同编码26S蛋白酶体的ATP酶亚基。26S蛋白酶体是一个大型蛋白质复合物，负责细胞内蛋白质的降解，主要通过泛素-蛋白酶体途径清除错误折叠或受损的蛋白质，以及调控细胞周期、信号传导和免疫反应等关键生物学过程。PSMC2基因编码的蛋白具有ATP酶活性，为蛋白酶体提供能量以展开并转运待降解的蛋白质至核心颗粒中进行水解。PSMC2在多种组织中广泛表达，尤其在增殖活跃的细胞（如癌细胞）中表达较高，因为其功能与细胞周期调控密切相关。PSMC2的突变可能导致蛋白酶体功能异常，进而引发蛋白质稳态失衡，与神经退行性疾病（如帕金森病和阿尔茨海默病）及某些癌症的发生发展相关。研究发现，PSMC2的过表达可能促进肿瘤细胞的增殖和存活，因其增强了异常蛋白的清除能力，帮助癌细胞抵抗应激；而降低PSMC2表达则可能导致蛋白质毒性积累，诱发细胞凋亡或自噬，但也可能因蛋白酶体功能不足而加剧神经退行性病变。PSMC家族成员的共性是均含有AAA-ATP酶结构域，能通过水解ATP为蛋白酶体提供机械力，且各成员在复合物中形成六聚体环状结构，协同完成底物识别、去折叠和转运。此外，PSMC2与其他家族成员（如PSMC1和PSMC4）相互作用，共同维持蛋白酶体的完整性和效率。研究还表明，PSMC2可能通过调控NF-κB等信号通路影响炎症和免疫反应，其表达水平的变化可能间接影响其他依赖蛋白酶体降解的蛋白质（如细胞周期蛋白和转录因子）的稳定性，从而广泛影响细胞功能。
The 26S proteasome is a multicatalytic proteinase complex with a highly ordered structure composed of 2 complexes, a 20S core and a 19S regulator. The 20S core is composed of 4 rings of 28 non-identical subunits; 2 rings are composed of 7 alpha subunits and 2 rings are composed of 7 beta subunits. The 19S regulator is composed of a base, which contains 6 ATPase subunits and 2 non-ATPase subunits, and a lid, which contains up to 10 non-ATPase subunits. Proteasomes are distributed throughout eukaryotic cells at a high concentration and cleave peptides in an ATP/ubiquitin-dependent process in a non-lysosomal pathway. An essential function of a modified proteasome, the immunoproteasome, is the processing of class I MHC peptides. This gene encodes one of the ATPase subunits, a member of the triple-A family of ATPases which have a chaperone-like activity. This subunit has been shown to interact with several of the basal transcription factors so, in addition to participation in proteasome functions, this subunit may participate in the regulation of transcription. This subunit may also compete with PSMC3 for binding to the HIV tat protein to regulate the interaction between the viral protein and the transcription complex. Alternative splicing results in multiple transcript variants encoding distinct isoforms. [provided by RefSeq, Mar 2011]
的26S蛋白酶体是一个multicatalytic蛋白酶复合带的2复合物构成的高度有序的结构，20S芯和19S调节器。 20S的核心是由4个环，28个非相同亚基组成; 2环由7个α亚和2环由7个β亚基。的19S调节器是由一个基地，它包含6 ATP酶亚基和2个非ATP酶亚基，和一个盖，其中含有多达10个非ATP酶亚基的。蛋白酶在整个真核细胞中分布以高浓度和裂开的肽在一个ATP /泛素依赖的过程在非溶酶体途径。修饰的蛋白酶，免疫蛋白酶，的一个重要功能是MHC I类肽的处理。该基因编码的ATP酶亚基之一，三A家族，其具有分子伴侣活性ATP酶的成员。这种亚单位已被证明与几个基础转录因子的相互作用是这样，除了在蛋白酶体功能的参与，这亚基可能参与转录的调节。此亚基也可以与PSMC3竞争结合的HIV Tat蛋白调节病毒蛋白和转录复杂的相互作用。在多个转录剪接变异体结果不同编码的亚型。 [由RefSeq的，2011年3月提供]
基因本体信息
PSMC2基因（以及对应的蛋白质）的细胞分布位置：
- 质膜
- 细胞质
- 细胞外
- 高尔基体
- 囊泡
- 细胞骨架
- 内质网
- 细胞核
- 内体
- 溶酶体
- 线粒体
PSMC2基因的本体（GO）信息：
| 名称 |
|---|
| 3050 Proteasome [PATH:hsa03050] |
| 5169 Epstein-Barr virus infection [PATH:hsa05169] |
| 名称 |
|---|
| Activation of APC/C and APC/C:Cdc20 mediated degradation of mitotic proteins |
| Activation of NF-kappaB in B cells |
| Adaptive Immune System |
| Antigen processing-Cross presentation |
| Antigen processing: Ubiquitination & Proteasome degradation |
| APC:Cdc20 mediated degradation of cell cycle proteins prior to satisfation of the cell cycle checkpoint |
| APC/C-mediated degradation of cell cycle proteins |
| APC/C:Cdc20 mediated degradation of mitotic proteins |
| APC/C:Cdc20 mediated degradation of Securin |
| APC/C:Cdh1 mediated degradation of Cdc20 and other APC/C:Cdh1 targeted proteins in late mitosis/early G1 |
| Apoptosis |
| Assembly of the pre-replicative complex |
| Asymmetric localization of PCP proteins |
| AUF1 (hnRNP D0) destabilizes mRNA |
| Autodegradation of Cdh1 by Cdh1:APC/C |
| Autodegradation of the E3 ubiquitin ligase COP1 |
| beta-catenin independent WNT signaling |
| C-type lectin receptors (CLRs) |
| Cdc20:Phospho-APC/C mediated degradation of Cyclin A |
| CDK-mediated phosphorylation and removal of Cdc6 |
| CDT1 association with the CDC6:ORC:origin complex |
| Cell Cycle |
| Cell Cycle Checkpoints |
| Cell Cycle, Mitotic |
| Class I MHC mediated antigen processing & presentation |
| CLEC7A (Dectin-1) signaling |
| Cross-presentation of soluble exogenous antigens (endosomes) |
| Cyclin A:Cdk2-associated events at S phase entry |
| Cyclin E associated events during G1/S transition |
| Dectin-1 mediated noncanonical NF-kB signaling |
| degradation of AXIN |
| Degradation of beta-catenin by the destruction complex |
| degradation of DVL |
| Degradation of GLI1 by the proteasome |
| Degradation of GLI2 by the proteasome |
| Disease |
| Diseases of signal transduction |
| DNA Replication |
| DNA Replication Pre-Initiation |
| Downstream signaling events of B Cell Receptor (BCR) |
| ER-Phagosome pathway |
| G1/S DNA Damage Checkpoints |
| G1/S Transition |
| Gene Expression |
| GLI3 is processed to GLI3R by the proteasome |
| Hedgehog 'off' state |
| Hedgehog 'on' state |
| Hedgehog ligand biogenesis |
| Hh mutants abrogate ligand secretion |
| Hh mutants that don't undergo autocatalytic processing are degraded by ERAD |
| HIV Infection |
| Host Interactions of HIV factors |
| Immune System |
| Infectious disease |
| Innate Immune System |
| M Phase |
| M/G1 Transition |
| Metabolism of amino acids and derivatives |
| Mitotic Anaphase |
| Mitotic G1-G1/S phases |
| Mitotic Metaphase and Anaphase |
| Orc1 removal from chromatin |
| p53-Dependent G1 DNA Damage Response |
| p53-Dependent G1/S DNA damage checkpoint |
| p53-Independent DNA Damage Response |
| p53-Independent G1/S DNA damage checkpoint |
| PCP/CE pathway |
| Programmed Cell Death |
| Regulation of activated PAK-2p34 by proteasome mediated degradation |
| Regulation of APC/C activators between G1/S and early anaphase |
| Regulation of Apoptosis |
| Regulation of DNA replication |
| Regulation of mitotic cell cycle |
| Regulation of mRNA stability by proteins that bind AU-rich elements |
| Regulation of ornithine decarboxylase (ODC) |
| Removal of licensing factors from origins |
| S Phase |
| SCF-beta-TrCP mediated degradation of Emi1 |
| SCF(Skp2)-mediated degradation of p27/p21 |
| Separation of Sister Chromatids |
| Signaling by Hedgehog |
| Signaling by the B Cell Receptor (BCR) |
| Signaling by Wnt |
| Stabilization of p53 |
| Switching of origins to a post-replicative state |
| Synthesis of DNA |
| TCF dependent signaling in response to WNT |
| Ubiquitin Mediated Degradation of Phosphorylated Cdc25A |
| Ubiquitin-dependent degradation of Cyclin D |
| Ubiquitin-dependent degradation of Cyclin D1 |
| Vif-mediated degradation of APOBEC3G |
| Vpu mediated degradation of CD4 |
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