HCSGD entry for IGF1R
1. General information
| Official gene symbol | IGF1R |
|---|---|
| Entrez ID | 3480 |
| Gene full name | insulin-like growth factor 1 receptor |
| Other gene symbols | CD221 IGFIR IGFR JTK13 |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0001965 | G-protein alpha-subunit binding | IEA | molecular_function |
| GO:0004713 | Protein tyrosine kinase activity | IDA TAS | molecular_function |
| GO:0004714 | Transmembrane receptor protein tyrosine kinase activity | IEA | molecular_function |
| GO:0005010 | Insulin-like growth factor-activated receptor activity | IDA | molecular_function |
| GO:0005158 | Insulin receptor binding | IDA | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005520 | Insulin-like growth factor binding | IDA | molecular_function |
| GO:0005524 | ATP binding | IEA | molecular_function |
| GO:0005886 | Plasma membrane | TAS | cellular_component |
| GO:0005887 | Integral component of plasma membrane | IC | cellular_component |
| GO:0005901 | Caveola | IEA | cellular_component |
| GO:0006468 | Protein phosphorylation | IEA | biological_process |
| GO:0006955 | Immune response | IMP | biological_process |
| GO:0007165 | Signal transduction | TAS | biological_process |
| GO:0007169 | Transmembrane receptor protein tyrosine kinase signaling pathway | IEA | biological_process |
| GO:0007409 | Axonogenesis | IEA | biological_process |
| GO:0007420 | Brain development | IEA | biological_process |
| GO:0008284 | Positive regulation of cell proliferation | TAS | biological_process |
| GO:0008286 | Insulin receptor signaling pathway | TAS | biological_process |
| GO:0010656 | Negative regulation of muscle cell apoptotic process | IEA | biological_process |
| GO:0014065 | Phosphatidylinositol 3-kinase signaling | IC | biological_process |
| GO:0016020 | Membrane | IDA | cellular_component |
| GO:0016021 | Integral component of membrane | IEA | cellular_component |
| GO:0018108 | Peptidyl-tyrosine phosphorylation | IDA TAS | biological_process |
| GO:0030010 | Establishment of cell polarity | IEA | biological_process |
| GO:0030238 | Male sex determination | IEA | biological_process |
| GO:0030335 | Positive regulation of cell migration | IMP | biological_process |
| GO:0030879 | Mammary gland development | IEA | biological_process |
| GO:0031017 | Exocrine pancreas development | IEA | biological_process |
| GO:0031994 | Insulin-like growth factor I binding | IPI | molecular_function |
| GO:0032467 | Positive regulation of cytokinesis | IEA | biological_process |
| GO:0033197 | Response to vitamin E | IEA | biological_process |
| GO:0042802 | Identical protein binding | IPI | molecular_function |
| GO:0043005 | Neuron projection | IEA | cellular_component |
| GO:0043066 | Negative regulation of apoptotic process | IDA | biological_process |
| GO:0043231 | Intracellular membrane-bounded organelle | IDA | cellular_component |
| GO:0043235 | Receptor complex | IDA | cellular_component |
| GO:0043409 | Negative regulation of MAPK cascade | IEA | biological_process |
| GO:0043410 | Positive regulation of MAPK cascade | IEA | biological_process |
| GO:0043548 | Phosphatidylinositol 3-kinase binding | IEA IPI | molecular_function |
| GO:0043559 | Insulin binding | IPI | molecular_function |
| GO:0043560 | Insulin receptor substrate binding | IEA IPI | molecular_function |
| GO:0045740 | Positive regulation of DNA replication | IMP | biological_process |
| GO:0046328 | Regulation of JNK cascade | IDA | biological_process |
| GO:0046777 | Protein autophosphorylation | IDA IEA | biological_process |
| GO:0048009 | Insulin-like growth factor receptor signaling pathway | IDA | biological_process |
| GO:0048015 | Phosphatidylinositol-mediated signaling | IDA | biological_process |
| GO:0051054 | Positive regulation of DNA metabolic process | IEA | biological_process |
| GO:0051262 | Protein tetramerization | IDA | biological_process |
| GO:0051291 | Protein heterooligomerization | IEA | biological_process |
| GO:0051389 | Inactivation of MAPKK activity | IDA | biological_process |
| GO:0051897 | Positive regulation of protein kinase B signaling | IEA | biological_process |
| GO:0051898 | Negative regulation of protein kinase B signaling | IEA | biological_process |
| GO:0060740 | Prostate gland epithelium morphogenesis | IEA | biological_process |
| GO:0090031 | Positive regulation of steroid hormone biosynthetic process | IEA | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.2072951636 | 0.0079126211 | 0.8780521403 | 0.1775516624 |
- 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 | Down | -0.6719955660 |
| GSE13712_SHEAR | Down | -0.8842835576 |
| GSE13712_STATIC | Down | -1.1218160410 |
| GSE19018 | Up | 0.3511785615 |
| GSE19899_A1 | Down | -0.5426303012 |
| GSE19899_A2 | Down | -1.0171172145 |
| PubMed_21979375_A1 | Down | -1.1670632534 |
| PubMed_21979375_A2 | Down | -0.6999070355 |
| GSE35957 | Up | 0.4621682955 |
| GSE36640 | Down | -0.1083589605 |
| GSE54402 | Down | -0.8379095324 |
| GSE9593 | Up | 0.1365618967 |
| GSE43922 | Down | -0.9490729209 |
| GSE24585 | Up | 0.5579833750 |
| GSE37065 | Down | -0.0239375322 |
| GSE28863_A1 | Up | 0.9688676093 |
| GSE28863_A2 | Up | 0.9692865396 |
| GSE28863_A3 | Up | 0.5119601931 |
| GSE28863_A4 | Down | -0.2452951689 |
| GSE48662 | Down | -0.0758535606 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
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- Drugs
Name | Drug | Accession number |
|---|---|---|
| Insulin Lispro | DB00046 | BTD00065 | BIOD00065 | DB01310 |
| Insulin Glargine | DB00047 | BTD00045 | BIOD00045 | DB01308 |
| Insulin Pork | DB00071 | BTD00031 | BIOD00031 |
| Mecasermin | DB01277 | - |
| Phosphoaminophosphonic Acid-Adenylate Ester | DB04395 | EXPT00524 |
| ATL1101 | DB05023 | - |
| XL228 | DB05184 | - |
| IMC-A12 | DB05759 | - |
| rhIGFBP-3 | DB05897 | - |
| INSM-18 | DB05900 | - |
| (4Z)-6-bromo-4-({[4-(pyrrolidin-1-ylmethyl)phenyl]amino}methylidene)isoquinoline-1,3(2H,4H)-dione | DB07156 | - |
| 3-[5-(1H-IMIDAZOL-1-YL)-7-METHYL-1H-BENZIMIDAZOL-2-YL]-4-[(PYRIDIN-2-YLMETHYL)AMINO]PYRIDIN-2(1H)-ONE | DB07474 | - |
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-100-5p | MIMAT0000098 | MIRT006429 | Luciferase reporter assay | Functional MTI | 21654750 |
| hsa-miR-100-5p | MIMAT0000098 | MIRT006429 | ELISA//GFP reporter assay//Immunoblot//Immunoprecipitaion//Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 21643012 |
| hsa-miR-122-5p | MIMAT0000421 | MIRT000364 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 19726678 |
| hsa-miR-122-5p | MIMAT0000421 | MIRT000364 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 23056576 |
| hsa-miR-122-5p | MIMAT0000421 | MIRT000364 | Reporter assay;qRT-PCR | Functional MTI | 20884628 |
| hsa-miR-223-3p | MIMAT0000280 | MIRT006244 | Luciferase reporter assay//Western blot | Functional MTI | 22073238 |
| hsa-miR-99a-5p | MIMAT0000097 | MIRT006145 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 21687694 |
| hsa-miR-133b | MIMAT0000770 | MIRT004460 | Luciferase reporter assay | Functional MTI | 19695767 |
| hsa-miR-145-5p | MIMAT0000437 | MIRT004931 | qRT-PCR//Western blot | Functional MTI | 19391107 |
| hsa-miR-7-5p | MIMAT0000252 | MIRT005364 | Flow//qRT-PCR//Western blot//Reporter assay;Other | Functional MTI | 20819078 |
| hsa-miR-7-5p | MIMAT0000252 | MIRT005364 | Luciferase reporter assay | Functional MTI | 22614005 |
| hsa-miR-138-5p | MIMAT0000430 | MIRT005691 | Luciferase reporter assay | Non-Functional MTI | 20819078 |
| hsa-miR-194-5p | MIMAT0000460 | MIRT005892 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 20979124 |
| hsa-miR-497-5p | MIMAT0002820 | MIRT006785 | Luciferase reporter assay | Functional MTI | 23453369 |
| hsa-miR-152-3p | MIMAT0000438 | MIRT006861 | Luciferase reporter assay//Western blot | Functional MTI | 22935141 |
| hsa-miR-139-5p | MIMAT0000250 | MIRT006942 | Luciferase reporter assay | Functional MTI | 22580051 |
| hsa-miR-376c-3p | MIMAT0000720 | MIRT006964 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 22747855 |
| hsa-miR-376a-3p | MIMAT0000729 | MIRT006965 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 22747855 |
| hsa-miR-181b-5p | MIMAT0000257 | MIRT007239 | Luciferase reporter assay | Functional MTI | 23431408 |
| hsa-miR-383-5p | MIMAT0000738 | MIRT007246 | Luciferase reporter assay | Functional MTI | 23564324 |
| hsa-miR-335-5p | MIMAT0000765 | MIRT018536 | Reporter assay;Western blot | Functional MTI | 21618216 |
| hsa-miR-215-5p | MIMAT0000272 | MIRT024453 | Microarray | Functional MTI (Weak) | 19074876 |
| hsa-miR-183-5p | MIMAT0000261 | MIRT025009 | Sequencing | Functional MTI (Weak) | 20371350 |
| hsa-miR-196a-5p | MIMAT0000226 | MIRT026064 | Sequencing | Functional MTI (Weak) | 20371350 |
| hsa-miR-192-5p | MIMAT0000222 | MIRT026729 | Microarray | Functional MTI (Weak) | 19074876 |
| hsa-miR-30a-5p | MIMAT0000087 | MIRT028606 | Proteomics | Functional MTI (Weak) | 18668040 |
| hsa-let-7d-5p | MIMAT0000065 | MIRT032181 | Sequencing | Functional MTI (Weak) | 20371350 |
| hsa-miR-1226-3p | MIMAT0005577 | MIRT036409 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-484 | MIMAT0002174 | MIRT041856 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-320a | MIMAT0000510 | MIRT044504 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-34a-5p | MIMAT0000255 | MIRT047346 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-92a-3p | MIMAT0000092 | MIRT049840 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-let-7e-5p | MIMAT0000066 | MIRT051489 | CLASH | Functional MTI (Weak) | 23622248 |
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- mirRecord
- mirRecord
MicroRNA name | mirBase ID | Target site number | MiRNA mature ID | Test method inter | MiRNA regulation site | Reporter target site | Pubmed ID |
|---|---|---|---|---|---|---|---|
| hsa-miR-99a-5p | MIMAT0000097 | 1 | hsa-miR-99a | 20484036 | |||
| hsa-miR-100-5p | MIMAT0000098 | 1 | hsa-miR-100 | {Western blot} | {knock down} | 20484036 | |
| hsa-miR-145-5p | MIMAT0000437 | NA | hsa-miR-145 | {Western blot} | {overexpression} | 19502786 | |
| hsa-miR-182-5p | MIMAT0000259 | NA | hsa-miR-182 | {Western blot} | {overexpression} | 19502786 |
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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 |
|---|---|
| 25148910 | The IGF1R/PI3K/Akt survival pathway in the heart of young rats can indeed be increased through exercise training |
| 24205274 | Inhibition of IGF-1R prevents ionizing radiation-induced primary endothelial cell senescence |
| 24205274 | Consistent with upregulation of these ligands, we found that X-ray exposure led to hyperphosphorylation of IGF-1R, the receptor for IGF-1 and -2 |
| 24205274 | Treatment with AG1024, an IGF-1R inhibitor, suppressed IR-induced upregulation of p53, p21/waf1, and SA-beta-gal |
| 24205274 | Together these findings suggest that IGF-1R is a key regulator of IR-induced accelerated senescence in a pathway that requires intact mTOR activity upstream of both p53 and p21/waf1 |
| 24055032 | METHOD: We have constructed multiple shRNA expression vectors of targeting EGFR, IGF1R and Bcl-xl, which were transfected to the CNE2 cells |
| 24055032 | The growth of the cells, cell cycle progression, apoptosis of the cells, senescent tumor cells and the proteins of EGFR, IGF1R and Bcl-xl were analyzed by MTT, flow cytometry, cytochemical therapy or Western blot |
| 24055032 | RESULTS: In group of simultaneously blocking EGFR, IGF1R and Bcl-xl genes, the mRNA of EGFR, IGF1R and Bcl-xl expression was decreased by (66 |
| 24055032 | CONCLUSIONS: Simultaneously blocking EGFR, IGF1R and Bcl-xl genes is capable of altering the balance between proliferating versus apoptotic and senescent cells in the favor of both of apoptosis and senescence and, therefore, the tumor cells regression |
| 23579096 | Activation of IGF-1R, after GA addition, promoted a reduction in the catalase content through the constitutive activation of Ras and erk1/2 proteins which were, in turn, responsible of the observed GA-induced senescence |
| 18938767 | Elevated insulin-like growth factor 1 receptor, hepatocyte growth factor receptor and telomerase protein expression in mild ulcerative colitis |
| 18938767 | METHODS: I-type insulin-like growth factor receptor (IGF1R), hepatocyte growth factor receptor (HGFR), telomerase reverse transcriptase (TERT) and telomerase associated protein (TP-1) expression were evaluated immunohistochemically on biopsy specimens from 11 mild, 11 moderate and 12 severe active inflammation of UC cases and from 10 normal colonic tissue cases |
| 18938767 | RESULTS: In mild inflammation, all observed parameters showed significantly elevated epithelial protein expression (IGF1R: 22 |
| 18938767 | In moderately active inflammation, only IGF1R expression was significantly higher (50 |
| 18938767 | In severe inflammation, all parameters showed decreased epithelial expression; IGF1R showed decreased mRNA expression, while HGFR was overexpressed and TERT showed a decreased tendency |
| 18938767 | CONCLUSIONS: The epithelial expression of IGF1R, HGFR and TERT/TP-1 is elevated in mildly active UC |
| 18451178 | Insulin-like growth factor-I (IGF-I) is a polypeptide hormone that can influence growth, differentiation, and survival of cells expressing the cognate type 1 receptor (IGF-IR) |
| 18451178 | To better understand cell autonomous IGF-IR signaling in the epithelial compartment of the prostate gland, we generated a conditional (Cre/loxP) prostate-specific IGF-IR knockout mouse model |
| 18451178 | In contrast to epidemiologic studies that established a correlation between elevated serum IGF-I and the risk of developing prostate cancer, we show that abrogation of IGF-IR expression in the dorsal and lateral prostate could activate extracellular signal-regulated kinase 1/2 signaling and cause cell autonomous proliferation and hyperplasia |
| 18451178 | Moreover, persistent loss of IGF-IR expression in dorsal and ventral lobes induced p53-regulated apoptosis and cellular senescence rescue programs, predicting that titration of IGF-IR signaling might facilitate growth of tumors with compromised p53 activity |
| 18451178 | Therefore, we crossed the mice carrying the prostate-specific IGF-IR knockout alleles into the transgenic adenocarcinoma of the mouse prostate model that is driven, in part, by T antigen-mediated functional inactivation of p53 |
| 18451178 | Consistent with our prediction, prostate epithelial-specific deletion of IGF-IR accelerated the emergence of aggressive prostate cancer when p53 activity was compromised |
| 18451178 | Collectively, these data support a critical role for IGF-IR signaling in prostate tumorigenesis and identify an important IGF-IR-dependent growth control mechanism |
| 17066600 | MATERIALS AND METHODS: I-type insulin-like growth factor receptor (IGF1R), hepatocyte derived growth factor receptor (HGFR), telomerase reverse transcriptase (TERT) and telomerase associated protein (TP-1) expression were evaluated immunohistochemically on formalin fixed paraffin embedded biopsy specimen from 10 mild, 10 moderate, and 10 severe active inflammation of ulcerative colitis and from 10 normal colonic tissue |
| 17066600 | In moderately active inflammation only IGF1R expression was significantly higher compared to normal and to mild inflammation (p <0 |
| 16263123 | The PDGF beta-receptor and insulin-like growth factor 1 receptor at the protein level also decreased but remained readily detectable |
| 15140969 | Concomitantly, these late-passage cervical cells exhibit an increase in sensitivity to IGF-1, including enhanced phosphorylation of the IGF receptor (IGF-R) and insulin receptor substrate as well as increased DNA synthesis (5-fold) and cell proliferation (3 |
| 15140969 | However, there was no change in the level of IGF-R in these cells (surface or total), and the cells did not synthesize IGF-1, indicating that these arms of the IGF pathway were independently regulated and not responsible for the augmented signaling |
| 9808148 | In addition, the level of the insulin-like growth factor type 1 receptor (IGF-1R) is increased in dex-treated cells |
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