PDF DatasheetHuman Anti-IDH1 Antibody Product Attributes
IDH1 Previously Observed Antibody Staining Patterns
Observed Subcellular, Organelle Specific Staining Data:
Anti-idh1 antibody staining is expected to be primarily localized to the cytosol and nuclear bodies. There is variability in either the signal strength or the localization of signal in nuclear bodies from cell to cell.
Observed Antibody Staining Data By Tissue Type:
Variations in IDH1 antibody staining intensity in immunohistochemistry on tissue sections are present across different anatomical locations. An intense signal was observed in cells in the seminiferous ducts in testis, chondrocytes in mesenchymal tissue, glandular cells in the adrenal gland, epididymis, gallbladder, prostate and seminal vesicle, Leydig cells in the testis and urothelial cells in the urinary bladder. More moderate antibody staining intensity was present in cells in the seminiferous ducts in testis, chondrocytes in mesenchymal tissue, glandular cells in the adrenal gland, epididymis, gallbladder, prostate and seminal vesicle, Leydig cells in the testis and urothelial cells in the urinary bladder. Low, but measureable presence of IDH1 could be seen inadipocytes in breast and mesenchymal tissue, glandular cells in the cervix, uterine, colon, fallopian tube and salivary gland, macrophages in lung, myoepithelial cells in the breast, ovarian stroma cells in the ovary, pneumocytes in lung, respiratory epithelial cells in the bronchus and nasopharynx and squamous epithelial cells in the esophagus. We were unable to detect IDH1 in other tissues. Disease states, inflammation, and other physiological changes can have a substantial impact on antibody staining patterns. These measurements were all taken in tissues deemed normal or from patients without known disease.
Observed Antibody Staining Data By Tissue Disease Status:
Tissues from cancer patients, for instance, have their own distinct pattern of IDH1 expression as measured by anti-IDH1 antibody immunohistochemical staining. The average level of expression by tumor is summarized in the table below. The variability row represents patient to patient variability in IHC staining.
| Sample Type | breast cancer | carcinoid | cervical cancer | colorectal cancer | endometrial cancer | glioma | head and neck cancer | liver cancer | lung cancer | lymphoma | melanoma | ovarian cancer | pancreatic cancer | prostate cancer | renal cancer | skin cancer | stomach cancer | testicular cancer | thyroid cancer | urothelial cancer |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Signal Intensity | – | ++ | – | – | + | + | – | – | – | – | – | + | + | +++ | – | – | + | – | – | – |
| IDH1 Variability | ++ | ++ | + | ++ | +++ | ++ | ++ | ++ | ++ | + | + | +++ | ++ | ++ | + | + | ++ | ++ | + | ++ |
| IDH1 General Information | |
|---|---|
| Alternate Names | |
| soluble Isocitrate dehydrogenase 1, soluble NADP+, IDH1 | |
| Molecular Weight | |
| 45-47kDa | |
| Chromosomal Location | |
| 2q33.3 | |
| Curated Database and Bioinformatic Data | |
| Gene Symbol | IDH1 |
| Entrez Gene ID | 3417 |
| Ensemble Gene ID | ENSG00000138413 |
| RefSeq Protein Accession(s) | NP_001269316, NP_005887, NP_001269315 |
| RefSeq mRNA Accession(s) | NM_001282386, NM_001282387 NM_005896 |
| RefSeq Genomic Accession(s) | NC_018913, NC_000002, NG_023319 |
| UniProt ID(s) | V9HWJ2, O75874 |
| UniGene ID(s) | V9HWJ2, O75874 |
| HGNC ID(s) | 5382 |
| Cosmic ID(s) | IDH1 |
| KEGG Gene ID(s) | hsa:3417 |
| PharmGKB ID(s) | PA29630 |
| General Description of IDH1. | |
| It recognizes a 45kDa protein, which is identified as isocitrate dehydrogenase (IDH1). It belongs to the isocitrate, isopropylmalate dehydrogenases family. IDH1 catalyzes the third step of the citric acid cycle, which involves the oxidative decarboxylation of isocitrate, forming ? -ketoglutarate, CO2 in a two-step reaction. The first step involves the oxidation of isocitrate to the intermediate oxalosuccinate, while the second step involves the production of ? -ketoglutarate. During this process, either NADH or NADPH is produced along with CO2. Recently, an inactivating mutation of IDH1 has been implicated in glioblastoma. IDH1 appears to function as a tumor suppressor that, when mutationally inactivated, contributes to tumorigenesis in part through induction of the HIF-1 pathway. | |
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