p14 ARF Antibody - #AF0229

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Product: p14 ARF Antibody
Catalog: AF0229
Description: Rabbit polyclonal antibody to p14 ARF
Application: WB IHC IF/ICC
Reactivity: Human
Prediction: Bovine, Horse, Rabbit, Dog
Mol.Wt.: 18kDa; 14kD(Calculated).
Uniprot: Q8N726
RRID: AB_2833404

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Related Downloads
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
WB 1:500-1:3000, IHC 1:50-1:200, IF/ICC: 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human
Prediction:
Bovine(80%), Horse(80%), Rabbit(80%), Dog(100%)
Clonality:
Polyclonal
Specificity:
p14 ARF Antibody detects endogenous levels of total p14 ARF.
RRID:
AB_2833404
Cite Format: Affinity Biosciences Cat# AF0229, RRID:AB_2833404.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

ARF; CDK4 inhibitor p16 INK4; CDK4I; CDKN2; CDKN2A; Cell cycle negative regulator beta; CMM2; Cyclin dependent kinase 4 inhibitor A; Cyclin dependent kinase inhibitor 2A; INK4; INK4a; Melanoma p16 inhibits CDK4; MLM; MTS 1; MTS1; Multiple tumor suppressor 1; p14; p16; p16 INK4a; p16INK4a; p19; P19ARF; TP16;

Immunogens

Immunogen:

A synthesized peptide derived from human p14 ARF, corresponding to a region within the internal amino acids.

Uniprot:

Q8N726(ARF_HUMAN) >>Visit HPA database.

Gene(ID):
CDKN2A(1029)
Description:
p14ARF an inhibitor of CDK4 kinase. 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. 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.
Sequence:
MVRRFLVTLRIRRACGPPRVRVFVVHIPRLTGEWAAPGAPAAVALVLMLLRSQRLGQQPLPRRPGHDDGQRPSGGAAAAPRRGAQLRRPRHSHPTRARRCPGGLPGHAGGAAPGRGAAGRARCLGPSARGPG

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Dog
100
Horse
80
Bovine
80
Rabbit
80
Pig
0
Sheep
0
Xenopus
0
Zebrafish
0
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - Q8N726 As Substrate

Site PTM Type Enzyme
T8 Phosphorylation P17252 (PRKCA)
T31 Phosphorylation
R115 Methylation
R120 Methylation
R122 Methylation
R129 Methylation

Research Backgrounds

Function:

Capable of inducing cell cycle arrest in G1 and G2 phases. Acts as a tumor suppressor. Binds to MDM2 and blocks its nucleocytoplasmic shuttling by sequestering it in the nucleolus. This inhibits the oncogenic action of MDM2 by blocking MDM2-induced degradation of p53 and enhancing p53-dependent transactivation and apoptosis. Also induces G2 arrest and apoptosis in a p53-independent manner by preventing the activation of cyclin B1/CDC2 complexes. Binds to BCL6 and down-regulates BCL6-induced transcriptional repression. Binds to E2F1 and MYC and blocks their transcriptional activator activity but has no effect on MYC transcriptional repression. Binds to TOP1/TOPOI and stimulates its activity. This complex binds to rRNA gene promoters and may play a role in rRNA transcription and/or maturation. Interacts with NPM1/B23 and promotes its polyubiquitination and degradation, thus inhibiting rRNA processing. Interacts with COMMD1 and promotes its 'Lys63'-linked polyubiquitination. Interacts with UBE2I/UBC9 and enhances sumoylation of a number of its binding partners including MDM2 and E2F1. Binds to HUWE1 and represses its ubiquitin ligase activity. May play a role in controlling cell proliferation and apoptosis during mammary gland development. Isoform smARF may be involved in regulation of autophagy and caspase-independent cell death; the short-lived mitochondrial isoform is stabilized by C1QBP.

PTMs:

Ubiquitinated in normal cells by TRIP12 via the ubiquitin fusion degradation (UFD) pathway, a process that mediates ubiquitination at the N-terminus, regardless of the absence of lysine residues. Ubiquitination leads to its proteasomal degradation. In cancer cells, however, TRIP12 is located in a different cell compartment, preventing ubiquitination and degradation.

Subcellular Location:

Nucleus>Nucleolus. Nucleus>Nucleoplasm.

Mitochondrion.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Subunit Structure:

Does not interact with cyclins, CDK1, CDK2, CDK4, CDK5 or CDK6. Binds to BCL6, E2F1, HUWE1, MDM2, MYC, NPM1/B23, TOP1/TOPOI and UBE2I/UBC9. Interacts with TBRG1 and COMMD1. Interacts with CDKN2AIP and E4F1. Interacts with CDK5RAP3 and MDM2; form a ternary complex involved in regulation of p53/TP53. Isoform smARF interacts with C1QBP. Interacts with NOP53; the interaction is direct and promotes ARF nucleoplasmic relocalization and ubiquitin-mediated proteasomal degradation.

Research Fields

· Cellular Processes > Cell growth and death > Cell cycle.   (View pathway)

· Cellular Processes > Cell growth and death > p53 signaling pathway.   (View pathway)

· Cellular Processes > Cell growth and death > Cellular senescence.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > Endocrine resistance.

· Human Diseases > Drug resistance: Antineoplastic > Platinum drug resistance.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Viral carcinogenesis.

· Human Diseases > Cancers: Overview > MicroRNAs in cancer.

· Human Diseases > Cancers: Specific types > Pancreatic cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Glioma.   (View pathway)

· Human Diseases > Cancers: Specific types > Melanoma.   (View pathway)

· Human Diseases > Cancers: Specific types > Bladder cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Chronic myeloid leukemia.   (View pathway)

· Human Diseases > Cancers: Specific types > Non-small cell lung cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Hepatocellular carcinoma.   (View pathway)

References

1). Effects of Ginsenoside Rg1 on the Biological Behavior of Human Amnion-Derived Mesenchymal Stem/Stromal Cells (hAD-MSCs). Stem Cells International, 2023 (PubMed: 36845966) [IF=4.3]

Application: WB    Species: Human    Sample: hAD-MSCs

Figure 6 Effects of ginsenoside Rg1 on the senescence of hAD-MSCs. (a) Senescent cells were detected by SA-β-Gal staining in the control, D-gal, Rg1, and Rg1+D-gal groups (×100). (b) hAD-MSC senescence rates were compared in the control, D-gal, Rg1, and Rg1+D-gal groups. (c, d) The expressions of cyclin D1, cyclin E1, CDK2, CDK4, p14ARF, p21CIP1, p53, and p16INK4a in hAD-MSCs were analyzed (c) and compared (d) by western blot in the control, D-gal, Rg1, and Rg1+D-gal groups. Representative images are shown. The red arrow indicates senescent hAD-MSCs stained with blue. Scale bars = 100 μm.
2). TET2-mediated Cdkn2A DNA hydroxymethylation in midbrain dopaminergic neurons injury of Parkinson's disease. HUMAN MOLECULAR GENETICS, 2020 (PubMed: 32037456) [IF=3.5]

Application: WB    Species: human    Sample: SH-SY5Y cell

Figure 4. Cdkn2A was mediated by TET2 in MPP+-induced SH-SY5Y cells. a Expression levels of Tet2 in shRNA-treated and mock groups in SH-SY5Y cell lines were detected by qRT-qPCR. b Western blot and quantification. SH-SY5Y cells were transfected with lentivirus-based-shRNA to regulate the expression of TET2. N = 3. Data are shown as the mean ± SD; ∗P < 0.05.c qRT-PCR assay was used to test the changes of Cdkn2A at mRNA level. N = 3. Data were expressed as the mean ± SD; ∗P < 0.05. d In the presence or absence MPP+, western blot and quantification to analysis the level of P14ARF and p16INK4A, which is one of the transcripts of Cdkn2A. N = 3. Data are shown as the mean ± SD; ∗P < 0.05, ∗∗P < 0.01.

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