PSMB9 (proteasome 20S subunit beta 9)
- symbol:
- PSMB9
- locus group:
- protein-coding gene
- location:
- 6p21.32
- gene_family:
- Proteasome (prosome, macropain) subunits
- alias symbol:
- RING12|beta1i|PSMB6i
- alias name:
- proteasome subunit β1i
- entrez id:
- 5698
- ensembl gene id:
- ENSG00000240065
- ucsc gene id:
- uc063wzi.1
- refseq accession:
- NM_002800
- hgnc_id:
- HGNC:9546
- approved reserved:
- 1991-12-18
PSMB9（蛋白酶体亚基β9型）是免疫蛋白酶体的一个关键组成部分，属于蛋白酶体β亚基家族。它主要在抗原呈递细胞中表达，负责将蛋白质降解为短肽片段，这些片段随后被MHC I类分子呈递到细胞表面，激活CD8+ T细胞，从而参与适应性免疫应答。PSMB9的表达受干扰素-γ（IFN-γ）的强烈诱导，表明其在炎症和免疫防御中起重要作用。该基因的突变可能导致抗原呈递功能受损，影响免疫监视，增加病毒感染或肿瘤发生的风险。研究发现，PSMB9的某些多态性与自身免疫性疾病（如类风湿性关节炎和1型糖尿病）的易感性相关。当PSMB9过表达时，可能增强抗原呈递效率，提高机体对病原体和肿瘤细胞的清除能力，但也可能加剧自身免疫反应；而降低表达则可能导致免疫应答减弱，增加感染和肿瘤风险。PSMB9属于蛋白酶体β亚基家族，该家族成员共同构成20S蛋白酶体的催化核心，负责蛋白质的降解。家族成员通常具有保守的催化残基，但PSMB9等免疫亚基在干扰素刺激下特异性表达，优化了对病毒和肿瘤抗原的呈递。此外，PSMB9还参与内质网相关降解（ERAD）途径，帮助清除错误折叠的蛋白质。其功能异常可能影响细胞蛋白质稳态，与神经退行性疾病（如帕金森病）的发病机制有关。总体而言，PSMB9在免疫调节和蛋白质质量控制中扮演多重角色，其表达水平的精确调控对维持机体健康至关重要。
The proteasome is a multicatalytic proteinase complex with a highly ordered ring-shaped 20S core structure. The core structure 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. 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 a member of the proteasome B-type family, also known as the T1B family, that is a 20S core beta subunit. This gene is located in the class II region of the MHC (major histocompatibility complex). Expression of this gene is induced by gamma interferon and this gene product replaces catalytic subunit 1 (proteasome beta 6 subunit) in the immunoproteasome. Proteolytic processing is required to generate a mature subunit. [provided by RefSeq, Mar 2010]
蛋白酶体是一个multicatalytic蛋白酶复杂与高度有序的环形20S核心结构。核心结构是由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。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。该基因编码的蛋白酶B型家族的成员，也称为T1B家族，这是一个20S核心β亚基。该基因位于MHC（主要组织相容性复合体）的II类区域。这个基因的表达是通过γ干扰素诱导的和该基因产物取代在免疫蛋白酶催化亚基1（蛋白酶测试6亚基）。需要蛋白水解加工以产生成熟亚基。 [由RefSeq的，2010年3月提供]
基因本体信息
PSMB9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
PSMB9基因的本体（GO）信息：
| 名称 |
|---|
| 3050 Proteasome [PATH:hsa03050] |
| 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 |
| 疾病名称 | 关系值 | NofPmids | NofSnps | 来源 |
| Diabetes Mellitus, Experimental | 0.08 | 1 | 0 | RGD |
| Peptic Esophagitis | 0.08 | 1 | 0 | RGD |
| Mammary Neoplasms | 0.08 | 1 | 0 | RGD |
| Diabetes Mellitus, Insulin-Dependent | 0.015287959 | 8 | 0 | BeFree_GAD |
| Psoriasis | 0.007729856 | 2 | 0 | BeFree_GAD_LHGDN |
| Ankylosing spondylitis | 0.006362715 | 8 | 0 | BeFree_GAD |
| Juvenile arthritis | 0.005276948 | 4 | 0 | BeFree_GAD |
| Multiple Sclerosis | 0.005005506 | 2 | 0 | BeFree_GAD |
| Uterine Cervical Neoplasm | 0.004734064 | 2 | 0 | GAD |
| Alzheimer's Disease | 0.004734064 | 2 | 0 | GAD |
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