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Validated All-in-One™ qPCR Primer for PYCARD(NM_013258.4) Search again
Product ID:
HQP099731
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ASC, CARD5, TMS, TMS-1, TMS1
Gene Description:
PYD and CARD domain containing
Target Gene Accession:
NM_013258.4(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 encodes an adaptor protein that is composed of two protein-protein interaction domains: a N-terminal PYRIN-PAAD-DAPIN domain (PYD) and a C-terminal caspase-recruitment domain (CARD). The PYD and CARD domains are members of the six-helix bundle death domain-fold superfamily that mediates assembly of large signaling complexes in the inflammatory and apoptotic signaling pathways via the activation of caspase. In normal cells, this protein is localized to the cytoplasm; however, in cells undergoing apoptosis, it forms ball-like aggregates near the nuclear periphery. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq].
Gene References into function
- Same as TMS1(target of methylation-induced silencing-1). TMS1/ASC found to be inactivated in association with promoter region methylation in human breast cancer cell lines and tumors.
- Proapoptotic CARD protein. Subcellular redistribution into perinuclear spherical structure appears to precede the downstream activation of a caspase-9-mediated apoptotic pathway. Does not activate NK-kB-dependent transcription.
- there are sites of protein binding and/or structural transitions define the boundaries of the unmethylated CpG island in normal cells and aberrant methylation overcomes these boundaries to direct change in chromatin structure, resulting in gene silencing
- The PYRIN-CARD protein ASC is an activating adaptor for caspase-1.
- ASC, which is composed of a PYD and a CARD, is up-regulated by inflammation and apoptosis in human neutrophils
- inflammasome comprises caspase-1, caspase-5, Pycard/Asc, and NALP1; a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta
- findings suggest that ASC modulates diverse NF-kappaB induction pathways by acting upon the IKK complex, implying a broad role for this and similar proteins containing PAAD domains in regulation of inflammatory responses
- Results suggest a direct role for aberrant methylation of the TMS1 gene in the progression of breast and gastric cancer involving down-regulation of the proapoptotic TMS1 gene.
- there is a cryopyrin signaling pathway activated through the induced proximity of ASC, which is negatively regulated by pyrin
- ASC is a mediator of NF-kappa B activation and Caspase-8-dependent apoptosis in an Ipaf signaling pathway
- gene silencing and dense methylation are tightly coupled events that affect individual chromosomal copies of TMS1 in an all-or-none manner
- Aberrant methylation of TMS1 is associated with pathogenesis of small cell, non small cell lung cancer and breast cancer
- Downregulated by aberrant methylation of Tms1 is associated with melanoma
- electrostatic interactions play an important role for the binding between PYRIN domains in ASC protein
- ASC binds by its caspase recruitment domain (CARD) to procaspase-1 and to adapter proteins involved in caspase-1 activation, thereby regulating cytokine pro-IL-1 beta activation by this protease in monocytic leukemia THP-1 cells.
- Methylation of ASC protein is associated with colorectal cancer
- Results suggest that apoptosis-associated speck-like protein (ASC) can function as an adaptor molecule for Bax and regulate a p53-Bax mitochondrial pathway of apoptosis.
- cellular location of pyrin mutant isoforms, in the presence or absence of ASC protein
- ASC has a role in cryopyrin-induced interleukin 1beta secretion in monocytic cells
- Methylation-mediated silencing of TMS1/ASC confers a survival advantage to ovarian tumor cells.
- A coherent interaction surface is identified in apoptosis-associated speck-like protein containing a caspase recruitment domain, establishing a molecular model of PYRIN domain (PYD)-PYD complexes with an important role for charge-charge interactions.
- caspase-8 plays an important role in the ASC-mediated NF-kappaB activation and IL-8 production, which actually induces physiologically relevant gene expression
- data suggest that both pyrin and cryopyrin are capable of assembling independent inflammasome complexes with ASC and procaspase-1, and activating caspase-1 via ASC oligomerization
- methylation of adjacent normal tissue occurs significantly more often in prostate cancer patients who later undergo biochemical recurrence, suggesting a role for inactivation of the ASC gene in the initial stages of aggressive disease
- Epigenetic silencing of TMS1 may contribute to carcinogenesis
- ASC expression correlates with IL-8 secretion and may play an important role in maintaining mucosal homeostasis
- Study demonstrates that methylation-mediated silencing of TMS1/ASC is a frequent event in prostate cancer.
- ASC, like death receptors, mediates two types of apoptosis depending on the cell type, in a manner involving caspase-8
- Hypermethylation of the proapoptotic gene TMS1 is associated with glioblastoma multiforme
- Correlation was observed between promoter methylation and loss of protein expression confirming our hypothesis that promoter methylation is an important mechanism for transcriptional silencing of these genes in breast cancer
- PSTPIP1 mutants require pyrin to induce formation of ASC pyroptosome, a molecular platform that recruits and activates caspase-1.
- The ASC/TMS1 gene is frequently silenced in colorectal cancer due to promoter hypermethylation.
- Relative copy numbers for the inflammasome mRNAs for ASC, caspase-1, NALP1, and Pypaf-7 were significantly lower in patients with septic shock compared with critically ill control subjects.
- The pyrin domain of the ASC and NALP1 proteins were simulated at two different pH values, 3.7 and 6.5, with two different force-field parameter sets, and the molecular dynamics simulation trajectories were compared to NMR experimental data
- Epigenetic silencing of TMS1 is associated with cancer
- ASC is expressed in renal glomeruli of patients with familial mediterranean fever. High local ASC expression results in speck formation and the specks from dying cells may persist in the extracellular space where they may nucleate amyloid.
- PYCARD appeared to play a central role in a stromal/hematopoietic cell coculture-dependent induction of genes relevant to the activation of caspase signaling and apoptosis
- P. gingivalis causes ASC- and NLRP3-dependent necrosis
- TMS1 is selectively down-regulated in the aberrant epithelial cells filling the lumen of the breast duct in a subset of primary Ductal carcinoma in situ lesions.