HCSGD entry for IVD
1. General information
| Official gene symbol | IVD |
|---|---|
| Entrez ID | 3712 |
| Gene full name | isovaleryl-CoA dehydrogenase |
| Other gene symbols | ACAD2 |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
This gene isn't in PPI subnetwork.
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0003995 | Acyl-CoA dehydrogenase activity | IEA | molecular_function |
| GO:0005759 | Mitochondrial matrix | IEA ISS TAS | cellular_component |
| GO:0006552 | Leucine catabolic process | IEA ISS | biological_process |
| GO:0008470 | Isovaleryl-CoA dehydrogenase activity | EXP IEA ISS | molecular_function |
| GO:0009083 | Branched-chain amino acid catabolic process | TAS | biological_process |
| GO:0031966 | Mitochondrial membrane | IEA | cellular_component |
| GO:0034641 | Cellular nitrogen compound metabolic process | TAS | biological_process |
| GO:0044281 | Small molecule metabolic process | TAS | biological_process |
| GO:0050660 | Flavin adenine dinucleotide 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 |
|---|---|---|---|
| 0.7737402986 | 0.1677329205 | 0.9999902473 | 0.7920520632 |
- 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 | Up | 0.1758201875 |
| GSE13712_SHEAR | Up | 0.2888879282 |
| GSE13712_STATIC | Down | -0.0264766425 |
| GSE19018 | Down | -0.0653332305 |
| GSE19899_A1 | Down | -0.1515343810 |
| GSE19899_A2 | Down | -0.0136577018 |
| PubMed_21979375_A1 | Down | -0.3188274277 |
| PubMed_21979375_A2 | Down | -0.0763474463 |
| GSE35957 | Up | 0.3478034528 |
| GSE36640 | Up | 0.4993309604 |
| GSE54402 | Down | -0.0457511207 |
| GSE9593 | Up | 0.0658565545 |
| GSE43922 | Down | -0.6575216742 |
| GSE24585 | Down | -0.1213465629 |
| GSE37065 | Down | -0.1659481010 |
| GSE28863_A1 | Down | -0.1122472537 |
| GSE28863_A2 | Down | -0.2463482680 |
| GSE28863_A3 | Down | -0.7807595388 |
| GSE28863_A4 | Up | 0.0118670386 |
| GSE48662 | Up | 0.3870516175 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Name | Drug | Accession number |
|---|---|---|
| Coenzyme a Persulfide | DB04036 | EXPT00989 |
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-124-3p | MIMAT0000422 | MIRT022872 | Microarray | Functional MTI (Weak) | 18668037 |
| hsa-miR-503-5p | MIMAT0002874 | MIRT041124 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-484 | MIMAT0002174 | MIRT041643 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-let-7e-5p | MIMAT0000066 | MIRT051477 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-let-7a-5p | MIMAT0000062 | MIRT052426 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
No target information from mirRecord
- mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 14 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 27192096 | Disc cell senescence decreased the number of functional cells in IVD |
| 26940203 | Cartilage end plates (CEP) degeneration plays an integral role in intervertebral disc (IVD) degeneration resulting from nutrient diffusion disorders |
| 26940203 | Therefore, the aim of this study was to investigate whether senescence is more prominent in human degenerative CEP and whether SIRT1-regulated CEP cells senescence in degenerative IVD as well as identify the signaling pathways that control that cell fate decision |
| 26826302 | The distinct sumoylation dynamics may help extend our understanding of the cell-specific regulation of the molecular basis that promotes cell survival in the hypoxic IVD |
| 26687460 | Repair of degenerated intervertebral discs (IVD) might be established via intradiscal delivery of biologic therapies |
| 26687460 | Polyester amide polymers (PEA) were evaluated for in vitro cytotoxicity and in vivo biocompatibility, and thereafter intradiscal application of PEA microspheres (PEAMs) in a canine model predisposed to IVD degeneration at long-term (6 months) follow-up |
| 26687460 | Intradiscal injection of a volume of 40 microL through 26 and 27G needles induced no degenerative changes in acanine model susceptible to IVD disease |
| 26687460 | These findings were not supported by other analyses (clinical signs, disc height index, T2 values, biomolecular and biochemical analyses, and IVD histopathology) |
| 26455958 | Intervertebral disc (IVD) degeneration is a complicated process that involves both age-related change and tissue damage caused by multiple stresses |
| 26455958 | In a degenerative IVD, cellular senescence accumulates and is associated with reduced proliferation, compromised self-repair, increased inflammatory response, and enhanced catabolic metabolism |
| 26455958 | In this review, we decipher the senescence mechanism of IVD degeneration (IVDD) by interpreting how aging coordinates with age-related, microenvironment-derived stresses in promoting disc cell senescence and accelerating IVDD |
| 26455958 | While acute disc injury, excessive mechanical overloading, diabetes, and chronic tobacco smoking contribute to the amplification of senescence-inducing stresses, the avascular nature of IVD impairs the immune-clearance of the senescent disc cells, which accumulate in cell clusters, demonstrate inflammatory and catabolic phenotypes, deteriorate disc microenvironment, and accelerate IVDD |
| 26455958 | Guidelines dedicated to avoiding or alleviating senescence-inducing stresses might decelerate cellular senescence and benefit patients with IVD degenerative diseases |
| 26341894 | IL-1beta is highly expressed in degenerative intervertebral disk (IVD) tissues and cells, and it has been shown to be involved in multiple pathological processes during disk degeneration, including inflammatory responses, matrix destruction, angiogenesis and innervation, cellular apoptosis, oxidative stress and cellular senescence |
| 24286133 | INTRODUCTION: Increased expression of the proinflammatory cytokine TNF-alpha in intervertebral discs (IVDs) leads to inflammation, which results in progressive IVD degeneration |
| 24286133 | We have previously reported that activation of Wnt-beta-catenin (hereafter called Wnt) signaling suppresses the proliferation of nucleus pulposus cells and induces cell senescence, suggesting that Wnt signaling triggers the process of degeneration of the IVD |
| 23316633 | OBJECTIVE: To summarize the role of cellular senescence and senescent secretary phenotype in the intervertebral disc (IVD) degeneration |
| 23316633 | METHODS: Relevant articles that discussed the roles of cellular senescence in the IVD degeneration were extensively reviewed, and retrospective and comprehensive analysis was performed |
| 23316633 | The senescent phenomenon during IVD degeneration, senescent secretary phenotype of the disc cells, senescent pathways within the IVD microenvironment, as well as the anti-senescent approaches for IVD regeneration were systematically reviewed |
| 23316633 | The accumulation of senescent cells not only decreases the self-renewal ability of IVD, but also deteriorates the disc microenvironment by producing more inflammatory cytokines and matrix degrading enzymes |
| 23316633 | More specific senescent biomarkers are required to fully understand the phenotype change of senescent disc cells during IVD degeneration |
| 23316633 | Molecular analysis of the senescent disc cells and their intracellular signaling pathways are needed to get a safer and more efficient anti-senescence strategy for IVD regeneration |
| 23316633 | CONCLUSION: Cellular senescence is an important mechanism by which IVD cells decrease viability and degenerate biological behaviors, which provide a new thinking to understand the pathogenesis of IVD degeneration |
| 21892804 | The adult human intervertebral disc (IVD) is normally avascular |
| 21885700 | Although understanding of the biologic basis of intervertebral disk (IVD) degeneration is rapidly advancing, the unique IVD environment presents challenges to the development and delivery of biologic treatments |
| 21885700 | IVD degeneration and associated pain have led to interest in pathologic innervation of the IVD and ultimately to the development of percutaneous devices to ablate afferent nerve endings in the posterior annulus |
| 21885700 | Injection of growth factors and mitogens may help overcome these degenerative changes in IVD phenotype, and these potential treatments are being explored in animal studies |
| 21885700 | Gene therapy is an elegant method to address changes in protein expression, but efforts to apply this technology to IVD degeneration are still at early stages |
| 20533544 | We hypothesize that the activation of WNT/beta-catenin signaling may lead to an increased breakdown of the matrix, thereby promoting IVD degeneration |
| 18681962 | Many cases are attributed to age-related degeneration of the intervertebral disc (IVD); however, age-related degeneration appears to occur at an accelerated rate in some individuals |
| 18681962 | We have previously demonstrated biomarkers of cellular senescence within the human IVD and suggested a role for senescence in IVD degeneration |
| 18681962 | We hypothesised that stress-induced premature senescence (SIPS) occurs within the IVD and here we have investigated the expression and production of caveolin-1, a protein that has been shown previously to be upregulated in SIPS |
| 18681962 | RESULTS: Caveolin-1 gene expression and protein expression were demonstrated within the human IVD for the first time |
| 18681962 | Its expression in IVD tissue and its association with the senescent phenotype suggest that caveolin-1 and SIPS may play a prominent role in the pathogenesis of IVD degeneration |
| 18433481 | INTRODUCTION: The avascular nature of the human intervertebral disc (IVD) is thought to play a major role in disc pathophysiology by limiting nutrient supply to resident IVD cells |
| 18433481 | In the human IVD, the central IVD cells at maturity are normally chondrocytic in phenotype |
| 17498290 | We hypothesised that this is due to accelerated cellular senescence, which causes fundamental changes in the ability of disc cells to maintain the intervertebral disc (IVD) matrix, thus leading to IVD degeneration |
| 17498290 | Expression of P16INK4A (increased in cellular senescence) was also investigated in IVD tissue by means of immunohistochemistry |
| 17498290 | Our findings indicate that disc cell senescence occurs in vivo and is accelerated in IVD degeneration |
| 17498290 | Furthermore, the senescent phenotype is associated with increased catabolism, implicating cellular senescence in the pathogenesis of IVD degeneration |
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