Product Name	CDKN2A/p19ARF
Chinese Name	p19ARF抑癌基因抗体
Alias	CD2A2_HUMAN; ARF; Cyclin dependent kinase inhibitor 2A; INK4; MTS1; P19.
Research Area	Tumour  Cell biology  Signal transduction  Apoptosis  Cyclin  transcriptional regulatory factor  Mitochondrion
Immunogen Species	Rabbit
Clonality	Polyclonal
React Species	(predicted: Mouse, Rat, )
Applications	ELISA=1:5000-10000 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500 （Paraffin sections need antigen repair） not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user.
Theoretical molecular weight	19kDa
Cellular localization	The nucleus Mitochondrion
Form	Liquid
Concentration	1mg/ml
immunogen	KLH conjugated synthetic peptide derived from mouse P19ARF: 101-160/169
Lsotype	IgG
Purification	affinity purified by Protein A
Buffer Solution	0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
Storage	Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
Attention	This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
PubMed	PubMed
Product Detail	P19ARF 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 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. 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. Subunit: 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. Subcellular Location: Nucleus, nucleolus. Nucleus, nucleoplasm. Tissue Specificity: Widely expressed with very low levels in kidney and colon. SWISS: Q64364 Gene ID: 12578 Database links: Entrez Gene: 12578 Mouse SwissProt: Q64364 Mouse Unigene: 4733 Mouse p19ARF是抑癌基因，通过干扰p53的功能，导致细胞周期调节紊乱和Apoptosis障碍，使细胞发生癌变，与多种Tumour的形成有关。 目前对p19ARF的研究虽然取得了很大的进展，但是还存在一些亟待解决的问题，如:p19ARF蛋白的表达调控还不是十分清楚;如何正确地认识并理解p19ARF的作用机制，p19ARF对Tumour发生的研究有重要的理论意义;目前的许多证据大部分来源于动物实验，p19ARF与人类Tumour的关系还需要进一步研究。

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