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Validated All-in-One™ qPCR Primer for ADAM10(NM_001110.3) Search again
Product ID:
HQP090369
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AD10, AD18, CD156c, CDw156, HsT18717, MADM, RAK, kuz
Gene Description:
ADAM metallopeptidase domain 10
Target Gene Accession:
NM_001110.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
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:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
Members of the ADAM family are cell surface proteins with a unique structure possessing both potential adhesion and protease domains. This gene encodes and ADAM family member that cleaves many proteins including TNF-alpha and E-cadherin. [provided by RefSeq].
Gene References into function
- Atrial fibrillation is associated with an increase in the expression of ADAM10 in the heart atrium
- [alpha]-Secretase ADAM10 as well as [alpha]APPs is reduced in platelets and CSF of Alzheimer disease patients.
- ADAM10 mRNA levels were twofold higher in the hippocampus and cerebellum of Alzheimer's disease patients compared to controls, but without relationship to the severity of anatomical damage.
- 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.
- Review. The mode of activation of EGFR in response to bacterial lipoteichoic acid involves cleavage of the transmembrane ligand HBEGF by ADAM 10.
- Our present findings suggest important implications for understanding CD44-dependent signal transduction and a potential role of PS/gamma-secretase activity in the functional regulation of adhesion molecules.
- gamma-secretase cleavage of CT99 is a prerequisite for BACE-mediated processing at Abeta-34 site and therefore, BACE and gamma-secretase activity can be mutually dependent.
- under inflammatory conditions, ADAM-10, expressed by perivascular macrophages, and ADAM-17, expressed by invading T cells, may actively contribute to the pathogenesis of inflammatory disorders of the CNS.
- variation at the ADAM10 gene locus is not associated with Creutzfeldt-Jakob disease
- gamma secretase is regulated by nicastrin
- cholesterol depletion triggers shedding of the human interleukin-6 receptor by ADAM10 and ADAM17
- gamma-secretase is engaged directly by Notch activation, which leads to diminished PS1 expression, suggesting a complex set of feedback interactions following Notch activation
- APH-1 plays a GXXXG-dependent scaffolding role in both the initial assembly and subsequent maturation and maintenance of the active gamma-secretase complex.
- Purified cholesterol-rich microdomains from a low-density membrane fraction demonstrate gamma-secretase/ADAM10 activity, indicating that amyloid beta protein production can take place in rafts.
- ADAM 10, a putative alpha-secretase involved in Notch signaling, was found in neurons of the perinatal cortex. During aging there is an increase in intraneuronal staining intensity and in the number of cortical nerve cells that contain the enzyme
- ADAM10 is the major alpha-secretase cleaving amyloid precursor protein, with TACE playing a minor role; neither ADAM10 nor TACE is involved in the shedding of angiotensin converting enzyme
- NRADD is an additional gamma-secretase substrate
- IL-8 induces shedding of EGFR ligands because of an ADAM10-dependent pathway in gastric cancer cells
- ADAM10 mediates constitutive and activated pro-BTC shedding
- Expression of a dominant-negative form of kuzbanian in transgenic mice leads to reduced T-cell receptor beta expression in double-negative thymocytes and to a partial block between the double-negative to double-positive stages of development.
- ADAM10 has a role in E-cadherin shedding and epithelial cell-cell adhesion, migration, and beta-catenin translocation
- Data suggest a simple mechanism for regulating ADAM10-mediated ephrin proteolysis, which ensures that only Eph bound ephrins are recognized and cleaved.
- High levels of Prpc C-terminal fragment (C1) are associated with the presence of the active ADAM 10 suggesting this zinc metalloprotease as a candidate for the cleavage of PrP(c) in the human brain.
- Result suggests that ADAM10 expression plays a role in the carcinogenesis of oral squamous cell carcinoma (OSCC) and proliferation of OSCC cells, independent of APP processing.
- EGF induces ADAM10-mediated CD44 cleavage through Rac1 and mitogen-activated protein kinase activation, and thereby promotes tumour cell migration and invasion.
- ADAM10 is a major determinant of HER2 shedding, the inhibition of which, may provide a novel therapeutic approach for treating a variety of breast cancers with active HER2 signaling.
- ADAM10 mediates cleavage of a receptor tyrosine phosphatase and regulation of beta catenin's transcriptional activity.
- ADAM10-mediated release of CD46 from apoptotic vesicles may represent a form of strategy to allow restricted complement activation to deal with modified self
- ADAM10 is the protease responsible for constitutive and regulated Pcdh gamma shedding events that modulate the cell adhesion role of Pcdh gamma.
- ADAM9 does not behave as a genuine alpha-secretase but rather acts as an important upstream regulator of ADAM10 activity.
- furin enhances alpha-secretase activity via the cleavage of ADAM10 and TACE, and attenuated furin activity is connected to the production of Abeta
- ADAM-10 transgenic mice display significantly elevated cortical cholinergic, glutaminergic and GABAergic presynaptic bouton densities at an early developmental time point.
- These findings suggest that ADAM10 represents an important molecular modulator of FasL-mediated cell death.
- ADAM10 and SPPL2a were identified as two proteases implicated in FasL processing and release of the FasL intracellular domain, which has been shown to be important for retrograde FasL signaling
- ADAM10 overexpression in colon cancer cells displaying endogenous L1-CAM enhanced L1-CAM cleavage and induced liver metastasis, and ADAM10 also enhanced metastasis in colon cancer cells stably transfected with L1-CAM.
- In human prostate cancer, the nuclear translocation of ADAM-10 coupled with the androgen receptor is involved in tumor growth and progression.
- the ADAM10 prodomain inhibits betacellulin shedding, demonstrating that it could be of potential use as a therapeutic agent to treat cancer.
- SPPL2a and SPPL2b mediate the intramembrane cleavage, whereas neither SPP nor SPPL3 is capable of processing the Bri2 N-terminal fragment.
- ADAM10 is identified as the TSHR cleavage enzyme and it is shown that TSH regulates its activation.
- ADAM10-mediated E-cadherin proteolysis leads to the impaired cohesion of keratinocytes observed in eczematous dermatitis.
- N-terminal domains of TIMPs alone are insufficient for the inhibition of ADAM10
- Nardilysin enhances TNF-alpha shedding through activation of not only TACE but ADAM10.
- ADAM10 and ADAM17 were identified as being responsible for the cytokine-induced shedding of CXCL16 in mesangila cell.
- N-glycosylation is crucial for ADAM10 processing and resistance to proteolysis, and results suggest that it is required for full-enzyme activity.
- ADAM10 is a novel regulator of vascular permeability and demonstrates a hitherto unknown function in the regulation of VE-cadherin-dependent endothelial cell functions and leukocyte transendothelial migration
- CXCL16 and ADAM10 are involved in the recruitment of T cells to the kidney
- The sheddase ADAM10 was identified as a membrane protease responsible for RAGE cleavage.
- ADAM10 was found to be present in human myoblasts and to be exclusively expressed in type I fibers, suggesting that it may be critical in muscle fiber differentiation.
- data show that ADAM10 and ADAM17 are critically involved in the tumor-associated proteolytic release of soluble MICA facilitating tumor immune escape
- ADAM10 and MMP9 to be involved in RAGE shedding.
- cleavage of C4.4A by ADAM10 and ADAM17 contributes to tumor progression
- tetraspanins regulate the activity of ADAM10 toward several substrates