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Validated All-in-One™ qPCR Primer for ADAM9(NM_003816.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
This gene encodes a member of the ADAM (a disintegrin and metalloprotease domain) family. Members of this family are membrane-anchored proteins structurally related to snake venom disintegrins, and have been implicated in a variety of biological processes involving cell-cell and cell-matrix interactions, including fertilization, muscle development, and neurogenesis. The protein encoded by this gene interacts with SH3 domain-containing proteins, binds mitotic arrest deficient 2 beta protein, and is also involved in TPA-induced ectodomain shedding of membrane-anchored heparin-binding EGF-like growth factor. Two alternative splice variants have been identified, encoding distinct isoforms. [provided by RefSeq].
Gene References into function
- ADAM9 is involved in monocyte fusion.
- The downregulated expression of ADAM9 may serve as a marker for anterior polar cataracts.
- cloning of a novel form of human ADAM9 (hADAM9s) which has an alpha-secretase activity for Amyloid Protein Precursor
- First evidence is presented of ADAM9 as an insulin-like growth factor binding protein-5 (IGFBP-5) protease produced and secreted by osteoblasts in culture, able to degrade IGFBP-5 with high potency, thereby regulating the critical activity of IGFBP-5.
- The results indicate that ADAM9, ADAM10, and ADAM17, members of the disintegrin and metalloprotease family, catalyze alpha-secretory cleavage and therefore act as alpha-secretases in A172 cells.
- Expression of ADAM-9 mRNA and protein in human breast cancer.
- Cytoplasmic ADAM9 overexpression is associated with poor differentiation in ductal adenocarcinoma
- ADAM9 overexpression enhances cell adhesion and invasion of non-small cell lung cancer cells via modulation of other adhesion molecules and changes in sensitivity to growth factors, thereby promoting metastatic capacity to the brain.
- In melanoma ADAM-9 protein expression appeared to be restricted to the melanoma cells within the invading front.
- In conclusion, our findings are consistent with the hypothesis that FHL-2 and ADAM-9 are important modulators of IGFBP-5 actions and are, in part, regulated in a coordinated manner in bone
- ADAM9 does not behave as a genuine alpha-secretase but rather acts as an important upstream regulator of ADAM10 activity.
- Intracellular ROS and/or hydrogen peroxide, generated by cell stress, regulate ADAM9 expression. ADAM9 may support prostate cancer cell survival and progression.
- These findings suggest that reactive oxygen species is a common mediator responsible for ADAM9 protein induction in human prostate cancer cells, downstream from androgen receptor, and stress response signaling.
- the ADAM-9 adhesive domain plays a role in regulating the motility of cells by interaction with beta1 integrins and modulates MMP synthesis.
- ADAM9 is overexpressed in prostate cancer cases and is an independent prognostic marker of PSA relapse-free survival following radical prostatectomy.
