|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for TYROBP(NM_003332.3) Search again
Powered by BiozBy 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:
|
|
| A | B |
|
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. |
|
Summary
This gene encodes a transmembrane signaling polypeptide which contains an immunoreceptor tyrosine-based activation motif (ITAM) in its cytoplasmic domain. The encoded protein may associate with the killer-cell inhibitory receptor (KIR) family of membrane glycoproteins and may act as an activating signal transduction element. This protein may bind zeta-chain (TCR) associated protein kinase 70kDa (ZAP-70) and spleen tyrosine kinase (SYK) and play a role in signal transduction, bone modeling, brain myelination, and inflammation. Mutations within this gene have been associated with polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL), also known as Nasu-Hakola disease. Its putative receptor, triggering receptor expressed on myeloid cells 2 (TREM2), also causes PLOSL. Two alternative transcript variants encoding distinct isoforms have been identified for this gene.
Gene References into function
- Mutations in two genes encoding different subunits of a receptor signaling complex (TYROBP and TREM2) result in an identical disease phenotype
- Myeloid abnormalities seen in KARAP/DAP12-transgenic mice indicate that KARAP/DAP12-driven signals are involved in inflammation & constitute an essential target to control resolution of inflammatory disorders based on monocytes/macrophages & neutrophils.
- DAP12 has a role in signal transduction, bone modeling, and brain myelination [review]
- CD158j in T cells functions as a costimulatory molecule through the JNK pathway independent of KARAP/DAP12 and DAP10.
- These results indicate an important role for DAP12-TREM2 signaling complex in the differentiation and function of osteoclasts.
- DAP12 association with natural cytotoxicity receptor NKp44 is required for activating properties and surface expression of NKp44 in natural killer (NK) cells.
- In clones that lack expression of KARAP/DAP12, stimulation of killer Ig-receptor KIR2DS2 does not induce cytotoxicity, whereas expression of KARAP/DAP12 is sufficient to convert a costimulatory KIR receptor into a stimulatory molecule.
- Splenic mature dendritic cells from transgenic mice with DAP12 overexpression are characterized by an impaired tolerogenic potential
- requirement by activated and expanded CD8+ T cells for DAP12 for direct killing
- Nasu-Hakola disease due to a DAP12 mutation 4.
- This review discusses the dual functionality of DAP12 and presents evidence that DAP12 can suppress as well as activate natural killer (NK) cells.
- This is the first case of Nasu-Hakola disease caused by compound heterozygosity for loss-of-function mutations in DAP12.
- KIR3DS1 associates with the ITAM-bearing adaptor, DAP12
- activation signals delivered via DAP12 can be counterbalanced by the adaptor NTAL
- Transcript analysis of DCs of PLOSL patients show that DAP12 deficient cells differentiated into DCs and responded to pathogenic stimuli. However, the DCs showed morphological differences due to defects in the actin filaments.