HCSGD entry for HSP90B2P
1. General information
| Official gene symbol | HSP90B2P |
|---|---|
| Entrez ID | 7190 |
| Gene full name | heat shock protein 90kDa beta (Grp94), member 2, pseudogene |
| Other gene symbols | GRP94P1 GRP94b HSP HSPCP2 TRA1P1 TRAP1 |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
This gene isn't in Literature mining network.
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0005524 | ATP binding | IEA | molecular_function |
| GO:0006457 | Protein folding | IEA | biological_process |
| GO:0006950 | Response to stress | IEA | biological_process |
| GO:0051082 | Unfolded protein binding | IEA | molecular_function |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.9892673645 | 0.2980471297 | 0.9999902473 | 1.0000000000 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
| Data source | Up or down | Log fold change |
|---|---|---|
| GSE11954 | - | - |
| GSE13712_SHEAR | - | - |
| GSE13712_STATIC | - | - |
| GSE19018 | - | - |
| GSE19899_A1 | - | - |
| GSE19899_A2 | - | - |
| PubMed_21979375_A1 | - | - |
| PubMed_21979375_A2 | - | - |
| GSE35957 | - | - |
| GSE36640 | - | - |
| GSE54402 | - | - |
| GSE9593 | - | - |
| GSE43922 | Down | -0.0497973281 |
| GSE24585 | Down | -0.1604227156 |
| GSE37065 | Down | -0.0487801555 |
| GSE28863_A1 | - | - |
| GSE28863_A2 | - | - |
| GSE28863_A3 | - | - |
| GSE28863_A4 | - | - |
| GSE48662 | - | - |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
No target information from mirTarBase
- mirRecord
No target information from mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 10 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 23742046 | Heat shock proteins (HSP) are molecular chaperones and have been implicated in longevity and aging in many species |
| 23742046 | The induction of HSP in aging could potentially maintain protein homeostasis and longevity by refolding the damaged proteins which accumulate during aging and are toxic to cells |
| 23742046 | HSP are shown to increase life span in model organisms such as Caenorhabditis elegans and decrease aging-related proteotoxicity |
| 23742046 | Thus, decrease in HSP in aging is associated with disruption of cellular homeostasis which causes diseases such as cancer, cell senescence and neurodegeneration |
| 23742046 | HSP levels are decreased with aging in most organs including neurons |
| 23742046 | This review enquires into the role of some of these pathways in longevity/aging along with HSP |
| 22917237 | Importantly, alterations in Hsp expression have been demonstrated to affect stem cell behavior including self-renewal, differentiation, sensitivity to environmental stress, and aging |
| 21932444 | A total of 13 proteins were up-regulated in CTP, including apoptosis-related cathepsin D (CD), annexin A1 and heat shock protein 27 (HSP 27), and seven proteins were down-regulated in CTP, including prohibitin (PHB) |
| 18438428 | Impairment of Hsp70 activity--using a pharmacological Hsp inhibitor or transfecting cells with an Hsp70-blocking antibody--restored the cellular response to mitochondrial apoptosis triggering |
| 15970415 | The major stress inducible Heat Shock Protein (HSP 72) confers myocardial protection from ischemia |
| 15970415 | A decreased ability to express HSP 72 during homeostatic disruptions has been suggested as a possible mechanism for the increased susceptibility of aged hearts to ischemic stress |
| 15970415 | Given that Caloric Restriction (CR) has been reported to reverse or delay age-associated cellular senescence, we examined the effect of CR on the ability of aged hearts to induce and accumulate HSP 72 |
| 15970415 | Immediately after heat stress, or 24 h later, the myocardium was examined for either activation of the heat shock transcription factor (HSF) or HSP 72 accumulation |
| 15970415 | Hearts from heat stressed CR animals demonstrated an increased HSF activation and an increased HSP 72 content when compared to hearts from heat stressed aged animals |
| 15970415 | The HSF response and HSP 72 content of the hearts from heat stressed aged CR animals was comparable to that observed in hearts from heat stressed adult animals |
| 15970415 | These results suggest CR may preserve the ability of the aged myocardium to activate and/or express HSP 72 |
| 15031001 | Heat shock proteins (Hsp) form the most ancient defense system in all living organisms on earth |
| 15031001 | Hsp interact with a number of cellular systems and form efficient cytoprotective mechanisms |
| 15031001 | We also give a survey of the most important elements of the apoptotic machinery and show the various modes of how Hsp interact with the apoptotic events in detail |
| 15031001 | Finally, we show the emerging variety of pharmacological interventions inhibiting or, just conversely, inducing Hsp and review the emergence of Hsp as novel therapeutic targets in anticancer protocols |
| 12470835 | RMHS increased the levels of these Hsp even in early passage young cells and were maintained high throughout their replicative lifespan |
| 11053669 | The heat shock response involving the family of stress-proteins or the so-called heat shock proteins (HSP), represents the quickest and highly conserved response to proteotoxic insults |
| 11053669 | Since repeated mild heat stress is able to prevent the onset of various age-related changes during cellular aging in vitro, we suggest that treatments which increase HSP expression should reduce the extent of accumulation of abnormal proteins during aging |
| 2764934 | Heat shock induction of HSP 89 is regulated in cellular aging |
| 2764934 | Heat shock (42 degrees C) markedly increased the synthesis of proteins with apparent molecular weights of 98, 89, 72, 50, 42 and 25 KDa, with HSP 89 and 72 being most prominent |
| 2764934 | For example, the synthesis rate of HSP 89 increased from a basal heat shock of young cells (PDL 18); in the old cells (PDL 51), the increase was from 1% to a maximum of 4% at 10-12 hrs after initiation of the heat shock |
| 2764934 | Western blot analysis showed that HSP 89 constituted approximately 2 and 10% of total cellular proteins in control and heat shocked (42 degrees C, 12-24 hrs) young cells; corresponding values for the old cells were 2 and 4 |
| 2764934 | Northern blot quantitation of the amount of mRNA hybridizable to cDNA probes of HSP 89 provided evidence that this age-dependent decrease in induction of HSP 89 in IMR-90 cells was attributable to a transcriptional/pre-translational mechanism |
| 2745427 | We showed that heat shock induced the synthesis of proteins with apparent molecular weights of 98,000, 89,000, 78,000, 72,000, 64,000, 50,000 and 25,000, with heat shock protein (HSP) 89 and 72 being most prominent |
| 2745427 | Canavanine induced the synthesis of the four high molecular weight HSPs, particularly HSP 89 and HSP 78, without noticeably enhancing synthesis of the low molecular weight HSPs |
| 2745427 | Using cells with defined population doubling levels, we observed a direct correlation of the inducibility of HSP synthesis and the replicative potential of the cells used |
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