Thermo Fisher Scientific p16INK4a Polyclonal Antibody
Human p16INK4a 단백질을 인식하는 Rabbit Polyclonal Antibody로, Western blot 등 다양한 응용에 적합. 항원 친화 크로마토그래피로 정제된 고순도 제품이며, 액상 형태로 제공. 세포주기 조절 및 종양 억제 관련 연구에 활용 가능.
- 판매단위
- pk
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Applications
- Western Blot (WB): 1:500–1:1,000
Product Specifications
| 항목 | 내용 |
|---|---|
| Species Reactivity | Human |
| Host / Isotype | Rabbit / IgG |
| Class | Polyclonal |
| Type | Antibody |
| Immunogen | Synthetic peptide corresponding to amino acids at the N-terminus of Human p16INK4a |
| Conjugate | Unconjugated |
| Form | Liquid |
| Concentration | 1 mg/mL |
| Purification | Antigen affinity chromatography |
| Storage Buffer | PBS, pH 7.2, with 50% glycerol |
| Contains | 0.02% sodium azide |
| Storage Conditions | Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles. |
| Shipping Conditions | Wet ice |
| RRID | AB_2802985 |
Product Specific Information
Purity is >95% by SDS-PAGE.
Target Information
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 structurally unrelated to the other variants.
This ARF product stabilizes the tumor suppressor protein p53 by interacting with and sequestering the E3 ubiquitin-protein ligase MDM2, preventing p53 degradation.
Despite structural and functional differences, the CDK inhibitor isoforms and ARF product share a common role in cell cycle G1 control through CDK4 and p53 regulation.
This gene is frequently mutated or deleted in various tumors and is known as an important tumor suppressor gene.
For Research Use Only.
Not for use in diagnostic procedures. Not for resale without express authorization.
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