HSP90AA1是热休克蛋白90(HSP90)家族的重要成员之一,属于分子伴侣蛋白家族。HSP90家族包括HSP90AA1(诱导型)、HSP90AB1(组成型)和HSP90B1(内质网型)等亚型,它们共同的特点是能够帮助蛋白质正确折叠、维持蛋白质稳定性并参与细胞应激反应。HSP90AA1主要在细胞质中表达,其表达水平在热应激或其他环境压力下显著升高。该基因编码的HSP90蛋白通过与客户蛋白(如激酶、转录因子和类固醇激素受体)结合,协助它们完成构象成熟和功能激活。HSP90AA1在多种细胞过程中发挥关键作用,包括信号转导、细胞周期调控、凋亡抑制和免疫应答。突变或异常表达可能严重影响其功能,例如某些突变会削弱其与ATP或客户蛋白的结合能力,导致蛋白质错误折叠和聚集,这可能引发神经退行性疾病或癌症。HSP90AA1的过表达常见于多种肿瘤,如乳腺癌、肺癌和前列腺癌,因为它能稳定致癌蛋白(如HER2、AKT和突变型p53),促进肿瘤细胞存活和增殖。相反,降低HSP90AA1表达或使用其抑制剂(如格尔德霉素)可诱导客户蛋白降解,抑制肿瘤生长。此外,HSP90AA1还参与病毒感染和炎症反应,例如在流感病毒复制中起辅助作用。该基因的表达水平受热休克因子1(HSF1)调控,在应激条件下HSF1激活并上调HSP90AA1表达。HSP90家族蛋白均依赖ATP水解来驱动构象变化,完成客户蛋白的折叠循环。由于其在疾病中的重要作用,HSP90AA1已成为癌症治疗的研究靶点,但其广泛功能也使得靶向治疗需谨慎以避免副作用。
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HSP90AA1基因(以及对应的蛋白质)的细胞分布位置:
HSP90AA1基因的本体(GO)信息:
| 名称 |
|---|
| 4141 Protein processing in endoplasmic reticulum [PATH:hsa04141] |
| 4151 PI3K-Akt signaling pathway [PATH:hsa04151] |
| 4621 NOD-like receptor signaling pathway [PATH:hsa04621] |
| 4612 Antigen processing and presentation [PATH:hsa04612] |
| 4915 Estrogen signaling pathway [PATH:hsa04915] |
| 4914 Progesterone-mediated oocyte maturation [PATH:hsa04914] |
| 5200 Pathways in cancer [PATH:hsa05200] |
| 5215 Prostate cancer [PATH:hsa05215] |
| 名称 |
|---|
| Anchoring of the basal body to the plasma membrane |
| Assembly of the primary cilium |
| Attenuation phase |
| Axon guidance |
| Binding and Uptake of Ligands by Scavenger Receptors |
| Cell Cycle |
| Cell Cycle, Mitotic |
| Cellular response to heat stress |
| Cellular responses to stress |
| Centrosome maturation |
| Constitutive Signaling by EGFRvIII |
| Constitutive Signaling by Ligand-Responsive EGFR Cancer Variants |
| Developmental Biology |
| Disease |
| Diseases of signal transduction |
| eNOS activation |
| eNOS activation and regulation |
| EPH-Ephrin signaling |
| EPHA-mediated growth cone collapse |
| Fcgamma receptor (FCGR) dependent phagocytosis |
| G2/M Transition |
| Gene Expression |
| HSF1 activation |
| HSF1-dependent transactivation |
| Immune System |
| Infectious disease |
| Influenza Infection |
| Influenza Life Cycle |
| Influenza Viral RNA Transcription and Replication |
| Innate Immune System |
| Loss of Nlp from mitotic centrosomes |
| Loss of proteins required for interphase microtubule organization from the centrosome |
| Metabolism |
| Metabolism of nitric oxide |
| Mitotic G2-G2/M phases |
| Organelle biogenesis and maintenance |
| PIWI-interacting RNA (piRNA) biogenesis |
| Recruitment of mitotic centrosome proteins and complexes |
| Regulation of actin dynamics for phagocytic cup formation |
| Regulation of PLK1 Activity at G2/M Transition |
| Regulatory RNA pathways |
| Scavenging by Class F Receptors |
| Sema3A PAK dependent Axon repulsion |
| Semaphorin interactions |
| Signal Transduction |
| Signaling by EGFR in Cancer |
| Signaling by EGFRvIII in Cancer |
| Signaling by ERBB2 |
| Signaling by Ligand-Responsive EGFR Variants in Cancer |
| Signaling by VEGF |
| Tetrahydrobiopterin (BH4) synthesis, recycling, salvage and regulation |
| Uptake and actions of bacterial toxins |
| Uptake and function of diphtheria toxin |
| VEGFA-VEGFR2 Pathway |
| VEGFR2 mediated vascular permeability |
| Vesicle-mediated transport |
| vRNP Assembly |
| 疾病名称 | 关系值 | NofPmids | NofSnps | 来源 |
| Mammary Neoplasms | 0.201357209 | 7 | 0 | BeFree_CTD_human_RGD |
| Neoplasm Metastasis | 0.123528744 | 14 | 0 | BeFree_CTD_human |
| HIV Infections | 0.121085767 | 5 | 0 | BeFree_CTD_human |
| Ki-1+ Anaplastic Large Cell Lymphoma | 0.120542884 | 3 | 0 | BeFree_CTD_human |
| Contact Dermatitis | 0.12 | 1 | 0 | CTD_human |
| Hypertension, Portal | 0.08 | 1 | 0 | RGD |
| Diabetes Mellitus, Experimental | 0.08 | 1 | 0 | RGD |
| Malignant neoplasm of breast | 0.012138939 | 37 | 0 | BeFree_GAD |
| Breast Carcinoma | 0.010043349 | 37 | 0 | BeFree |
| melanoma | 0.008977445 | 14 | 0 | BeFree_LHGDN |
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