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Validated All-in-One™ qPCR Primer for INPP5D(NM_001017915.2) Search again
Product ID:
HQP009754
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
SHIP, SHIP-1, SHIP1, SIP-145, hp51CN, p150Ship
Gene Description:
inositol polyphosphate-5-phosphatase D
Target Gene Accession:
NM_001017915.2(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
This gene is a member of the inositol polyphosphate-5-phosphatase (INPP5) family and encodes a protein with an N-terminal SH2 domain, an inositol phosphatase domain, and two C-terminal protein interaction domains. Expression of this protein is restricted to hematopoietic cells where its movement from the cytosol to the plasma membrane is mediated by tyrosine phosphorylation. At the plasma membrane, the protein hydrolyzes the 5' phosphate from phosphatidylinositol (3,4,5)-trisphosphate and inositol-1,3,4,5-tetrakisphosphate, thereby affecting multiple signaling pathways. Overall, the protein functions as a negative regulator of myeliod cell proliferation and survival. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.
Gene References into function
- implicated as regulator of histamine release in basophils
- SHIP localization to membrane receptors and subsequent activation along with the observed inability of SHIP -/- neutrophils to exhibit enhanced apoptosis with the stimulus combination.
- Association of SHIP with releasability in human basophils.
- data demonstrate that CD16 engagement on NK cells induces membrane targeting and activation of SHIP-1, which acts as negative regulator of antibody-dependent cellular cytotoxicity function
- SHIP-1 contributes to degradation of phosphatidylinositol trisphosphate (PI(3,4,5)P3) in T cells and thus influences signaling away from PI(3,4,5)P3-dependent effectors toward effectors that are exclusively driven by phosphatidylinositol 3,4-bisphosphate
- SHIP expression appears to be differently altered in the early and late stages of differentiation of BCR-ABL-transformed cells
- SHIP-1 and Lyn have roles in the negative regulation of M-CSF-R-induced Akt activation
- SHIP positively, rather than negatively, regulates in vitro membrane recruitment of pleckstrin homology domain-containing signaling proteins Bam32 and TAPP2, which therefore specify a distinct wave of phosphatidylinositol 3-kinase signaling in B cells.
- SHIP1 and Lyn have roles as negative regulators of integrin alpha(IIb)beta(3) adhesive and signaling function
- SHIP1 and SHIP2 interact preferentially with Tec and inactivate it by de-phosphorylation of local PtdIns 3,4,5-P(3) and inhibition of Tec membrane localization
- SHIP1 negatively regulates monokine-induced NK cell IFN-gamma production in vitro and in vivo and provide the first molecular explanation for an important functional distinction observed between CD56bright and CD56dim human NK subsets.
- SHIP has a negative regulatory role in TLR2-induced neutrophil activation and in the development of related in vivo neutrophil-dependent inflammatory processes, such as acute lung injury in transgenic mice.
- Heterologous activation of SHIP by non-G-protein-coupled receptor-mediated routes can impinge on PI3K-dependent signaling pathways activated by independently ligated G-protein-coupled chemokine receptors.
- SHIP1 is necessary for FcgammaRIIB to negatively regulate B cell activation.
- Upregulated in oral mucosa during chronic periodontitis compared to its level during gingival health.
- Study showed H2O2-induced IKK activation in leukemic cells is mediated by SHIP-1; Jurkat cells expressing SHIP-1 are more resistant to H2O2-induced apoptosis than parental cells, suggesting SHIP-1 has an important role in leukemic cell responses to ROS
- Our results indicate that SHIP1 is involved, in a Src kinase-dependent manner, in the early signaling events observed upon the cross-linking of CD32a in human neutrophils.
- SHIP phosphorylation in stimulated human basophils undergoes modest nonspecific desensitization that persists despite dissociation of the desensitizing antigen, resulting in an immunologic memory of prior stimulation.
- SHIP1 not only acts as a negative player in T-cell lines proliferation, but also regulates critical pathways, such as NF-kappaB (nuclear factor kappaB) activation.
- Gene structure, expression profiling and mutation analysis of the tumour suppressor SHIP1 in Caucasian acute myeloid leukaemia