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Validated All-in-One™ qPCR Primer for CSTB(NM_000100.3) Search again
Product ID:
HQP003388
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CPI-B, CST6, EPM1, EPM1A, PME, STFB, ULD
Gene Description:
cystatin B
Target Gene Accession:
NM_000100.3(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
The cystatin superfamily encompasses proteins that contain multiple cystatin-like sequences. Some of the members are active cysteine protease inhibitors, while others have lost or perhaps never acquired this inhibitory activity. There are three inhibitory families in the superfamily, including the type 1 cystatins (stefins), type 2 cystatins and kininogens. This gene encodes a stefin that functions as an intracellular thiol protease inhibitor.
Gene References into function
- Oligonucleotides containing EPM1 repeat adopt secondary structures that may facilitate strand slippage thereby causing the expansion.
- Intramolecular i-motif structure at acidic pH for progressive myoclonus epilepsy (EPM1) repeat d(CCCCGCCCCGCG)n.
- analysed eight markers flanking CSTB(GT10-D21S1890-D21S1885-D21S2040-D21S1259- CSTB-D21S1912-PFKL-D21S171) and one intragenic variant in the CSTB 3' UTR (A2575G)
- first demonstration of cysteine protease activity being regulated by CSTB activity in a biological context; effects of decreased CSTB activity in EPM1 pathogenesis may be mediated by cathepsins through increased activity of cathepsins S and L
- By using ThT fluorescence, X-ray diffraction, and atomic force microscopy (AFM), it has been shown that human stefins A and B (subfamily A of cystatins) form amyloid fibrils
- Protein and mRNA levels of stefin B (p= 0.007), but not cystatin C, were significantly lower in atypical compared with benign meningiomas
- Prefibrillar oligomers/aggregates of stefin B also increase the surface pressure at an air-water interface, i.e. they have amphipathic character and are surface seeking.
- These data show that cystatin B inhibits bone resorption by down-regulating intracellular cathepsin K activity despite increased osteoclast survival.
- Chimeras of stefinA and B have been prepared and guanidine denaturation curves and folding rates have been examined.
- Study shows that copper binding by stefin B inhibits the amyloid fibril formation and, to a lesser degree, the initial aggregation.
- only stefins A and B, i.e. type I cystatins, are up-regulated in lung tumours and thus able to counteract harmful tumour-associated proteolytic activity
- Several alternatively spliced CSTB isoforms were identified in patients with progressive myoclonus epilepsy of Unverricht-Lundborg type .
- Results describe the influence of pH and trifluoroethanol on amyloid fibril growth and morphology from human stefin B.
- cystatin B in vivo has a polymeric structure sensitive to the redox environment and that overexpression of the protein generates aggregates.
- CSTB is specifically overexpressed in most HCCs and is also elevated in the serum of a large proportion of HCC patients
- Data show that wild-type stefin B and its Y31 isoform are able to form pores in planar lipid bilayers, whereas the G4R isoform destroys the bilayer by a non pore-forming process.
- The mechanism of amyloid-fibril formation by stefin B: temperature and protein concentration dependence of the rates;the observed kinetics follow the nucleation and growth behavior observed for many other amyloidogenic proteins.
- potential role for CSTB in HIV replication in placental macrophages