PDF DatasheetHuman Anti-ASRGL1 Antibody Product Attributes
ASRGL1 Previously Observed Antibody Staining Patterns
Observed Subcellular, Organelle Specific Staining Data:
Anti-ASRGL1 antibody staining is expected to be primarily localized to the microtubules and nucleoplasm.
Observed Antibody Staining Data By Tissue Type:
Variations in ASRGL1 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, glandular cells in the cervix and uterine, endometrium, epididymis and fallopian tube. More moderate antibody staining intensity was present in cells in the seminiferous ducts in testis, glandular cells in the cervix and uterine, endometrium, epididymis and fallopian tube. Low, but measureable presence of ASRGL1 could be seen in cells in the granular layer in cerebellum, cells in the tubules in kidney, glandular cells in the appendix, colon, duodenum, gallbladder, prostate and seminal vesicle, glial cells in the cerebral cortex, Leydig cells in the testis, neuronal cells in the caudate nucleus and cerebral cortex, neuropil in cerebral cortex, respiratory epithelial cells in the bronchus and nasopharynx, smooth muscle cells in the smooth muscle and urothelial cells in the urinary bladder. We were unable to detect ASRGL1 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 ASRGL1 expression as measured by anti-ASRGL1 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 | + | – | – | – | +++ | + | – | – | – | – | – | ++ | – | + | ++ | – | – | + | – | – |
| ASRGL1 Variability | +++ | ++ | ++ | ++ | ++ | ++ | ++ | + | + | + | + | ++ | ++ | ++ | ++ | + | ++ | ++ | ++ | + |
| ASRGL1 General Information | |
|---|---|
| Alternate Names | |
| L-asparaginase, ASRGL1 | |
| Molecular Weight | |
| 17-25kDa | |
| Chromosomal Location | |
| 11q12.3 | |
| Curated Database and Bioinformatic Data | |
| Gene Symbol | ASRGL1 |
| Entrez Gene ID | 80150 |
| Ensemble Gene ID | ENSG00000162174 |
| RefSeq Protein Accession(s) | XP_011543568, NP_079356, XP_005274362, XP_016873843, XP_011543567, NP_001077395, XP_005274363 |
| RefSeq mRNA Accession(s) | XM_005274305, XM_017018354, XR_001747982, NM_025080, XM_011545265, XM_005274306, XM_011545266, NM_001083926 |
| RefSeq Genomic Accession(s) | NC_000011, NC_018922 |
| UniProt ID(s) | A0A024R573, Q7L266 |
| UniGene ID(s) | A0A024R573, Q7L266 |
| HGNC ID(s) | 16448 |
| Cosmic ID(s) | ASRGL1 |
| KEGG Gene ID(s) | hsa:80150 |
| PharmGKB ID(s) | PA25059 |
| General Description of ASRGL1. | |
| ASRGL1 (Asparaginase-like protein 1), also known as CRASH, is a 308 amino acid protein belonging to the Ntn-hydrolase family. Asparaginases utilize asparagine as a substrate to produce aspartic acid and ammonia. ASRGL1 has been identified as a autoantigenic protein that is present in the mid-piece of sperm after obstruction of the male reproductive tract. ASRGL1 is expressed highly in testis, but is also expressed in brain, kidney and gastrointestinal tissues. High levels of ASRGL1 have also been identified in ovarian, uterine and mammary tumors in comparison with normal tissues of the same origin. | |
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