p16/p53/SMAD4 FISH Probe
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More Files
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Specification
Probe 2
Name: p53
Size: Approximately 190kb
Fluorophore: FITC
Location: 17p13.1Product Description
Labeled FISH probes for identification of gene amplification using Fluoresecent In Situ Hybridization Technique. (Technology)
Probe 1
Name: p16
Size: Approximately 110kb
Fluorophore: TexRed
Location: 9p21Probe 3
Name: SMAD4
Size: Approximately 250kb
Fluorophore: Cy5
Location: 18q21.2Origin
Human
Source
Genomic DNA
Reactivity
Human
Notice
We strongly recommend the customer to use FFPE FISH PreTreatment Kit 1 (Catalog #: KA2375 or KA2691) for the pretreatment of Formalin-Fixed Paraffin-Embedded (FFPE) tissue sections.
Regulation Status
For research use only (RUO)
Quality Control Testing
Representative images of normal human cell (lymphocyte) stain with the triple color FISH probe. The left image is chromosomes at metaphase, and the right image is an interphase nucleus.
Supplied Product
DAPI Counterstain (1500 ng/mL ) 250 uL
Storage Instruction
Store at 4°C in the dark.
Note
Hybridization position of the probes on the chromosome.
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Applications
Fluorescent In Situ Hybridization (Cell)
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Gene Info — CDKN2A
Entrez GeneID
1029Gene Name
CDKN2A
Gene Alias
ARF, CDK4I, CDKN2, CMM2, INK4, INK4a, MLM, MTS1, TP16, p14, p14ARF, p16, p16INK4, p16INK4a, p19
Gene Description
cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4)
Gene Ontology
HyperlinkGene Summary
This gene generates several transcript variants which differ in their first exons. At least three alternatively spliced variants encoding distinct proteins have been reported, two of which encode structurally related isoforms known to function as inhibitors of CDK4 kinase. The remaining transcript includes an alternate first exon located 20 Kb upstream of the remainder of the gene; this transcript contains an alternate open reading frame (ARF) that specifies a protein which is structurally unrelated to the products of the other variants. This ARF product functions as a stabilizer of the tumor suppressor protein p53 as it can interact with, and sequester, MDM1, a protein responsible for the degradation of p53. In spite of the structural and functional differences, the CDK inhibitor isoforms and the ARF product encoded by this gene, through the regulatory roles of CDK4 and p53 in cell cycle G1 progression, share a common functionality in cell cycle G1 control. This gene is frequently mutated or deleted in a wide variety of tumors, and is known to be an important tumor suppressor gene. [provided by RefSeq
Other Designations
CDK4 inhibitor p16-INK4|OTTHUMP00000021147|OTTHUMP00000021148|cell cycle negative regulator beta|cyclin-dependent kinase inhibitor 2A|cyclin-dependent kinase inhibitor p16|multiple tumor suppressor 1
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Gene Info — SMAD4
Entrez GeneID
4089Gene Name
SMAD4
Gene Alias
DPC4, JIP, MADH4
Gene Description
SMAD family member 4
Gene Ontology
HyperlinkGene Summary
mothers against decapentaplegic homolog 4|OTTHUMP00000163548|SMAD
Other Designations
MAD, mothers against decapentaplegic homolog 4|OTTHUMP00000163548|SMAD, mothers against DPP homolog 4|deleted in pancreatic carcinoma locus 4|mothers against decapentaplegic homolog 4|mothers against decapentaplegic, Drosophila, homolog of, 4
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Gene Info — TP53
Entrez GeneID
7157Gene Name
TP53
Gene Alias
FLJ92943, LFS1, TRP53, p53
Gene Description
tumor protein p53
Gene Ontology
HyperlinkGene Summary
This gene encodes tumor protein p53, which responds to diverse cellular stresses to regulate target genes that induce cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. p53 protein is expressed at low level in normal cells and at a high level in a variety of transformed cell lines, where it's believed to contribute to transformation and malignancy. p53 is a DNA-binding protein containing transcription activation, DNA-binding, and oligomerization domains. It is postulated to bind to a p53-binding site and activate expression of downstream genes that inhibit growth and/or invasion, and thus function as a tumor suppressor. Mutants of p53 that frequently occur in a number of different human cancers fail to bind the consensus DNA binding site, and hence cause the loss of tumor suppressor activity. Alterations of this gene occur not only as somatic mutations in human malignancies, but also as germline mutations in some cancer-prone families with Li-Fraumeni syndrome. Multiple p53 variants due to alternative promoters and multiple alternative splicing have been found. These variants encode distinct isoforms, which can regulate p53 transcriptional activity. [provided by RefSeq
Other Designations
p53 antigen|p53 transformation suppressor|p53 tumor suppressor|phosphoprotein p53|transformation-related protein 53
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Interactome
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Pathway
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Disease
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