RUNX1 Rabbit Polyclonal Antibody
Frequently bought together (2)
Other products for "RUNX1"
Specifications
Product Data | |
Applications | ICC/IF, IHC, WB |
Recommended Dilution | WB 1:500 - 1:2000;IHC 1:50- 1:200;IF 1:50- 1:200 |
Reactivities | Human, Mouse, Rat |
Host | Rabbit |
Isotype | IgG |
Clonality | Polyclonal |
Immunogen | A synthetic peptide of human RUNX1 |
Formulation | Store at -20C or -80C. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3 |
Concentration | lot specific |
Purification | Affinity purification |
Conjugation | Unconjugated |
Storage | Store at -20°C as received. |
Stability | Stable for 12 months from date of receipt. |
Gene Name | runt related transcription factor 1 |
Database Link | |
Background | AML1 (also known as Runx1, CBFA2, and PEBP2aB) is a member of the core binding factor (CBF) family of transcription factors. It is required for normal development of all hematopoietic lineages. AML1 forms a heterodimeric DNA binding complex with its partner protein CBFβ and regulates the expression of cellular genes by binding to promoter and enhancer elements. AML1 is commonly translocated in hematopoietic cancers: chromosomal translocations include t(8;21) AML1-ETO, t(12;21) TEL-AML, and t(8;21) AML-M2. Phosphorylation of AML1 on several potential serine and threonine sites, including Ser249, is thought to occur in an Erk-dependent manner. |
Synonyms | AML1; AML1-EVI-1; AMLCR1; CBFA2; EVI-1; PEBP2aB |
Reference Data | |
Protein Families | Druggable Genome, ES Cell Differentiation/IPS, Transcription Factors |
Protein Pathways | Acute myeloid leukemia, Chronic myeloid leukemia, Pathways in cancer |
Documents
Product Manuals |
FAQs |
SDS |
{0} Product Review(s)
0 Product Review(s)
Submit review
Be the first one to submit a review
Product Citations
*Delivery time may vary from web posted schedule. Occasional delays may occur due to unforeseen
complexities in the preparation of your product. International customers may expect an additional 1-2 weeks
in shipping.