Recombinant Human Core-binding factor subunit beta (CBFB)

Code CSB-EP623835HU
MSDS
Size $224
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  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
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Product Details

Purity
Greater than 90% as determined by SDS-PAGE.
Target Names
CBFB
Uniprot No.
Research Area
Epigenetics and Nuclear Signaling
Alternative Names
CBF b; CBF beta; CBF-beta; CBFB; CBFbeta; Core binding factor beta subunit; core binding factor subunit beta; Core-binding factor subunit beta; Core-binding factor, beta subunit (CBFB), transcript variant 2; PEA 2; PEA2; PEA2 beta; PEA2-beta; PEA2beta; PEBB_HUMAN; PEBP 2B; PEBP2 beta; PEBP2-beta; PEBP2B; PEBP2beta; Polyomavirus enhancer binding protein 2 beta subunit ; Polyomavirus enhancer-binding protein 2 beta subunit; SL3 3 enhancer factor 1 beta subunit; SL3 3 enhancer factor 1 subunit beta; SL3-3 enhancer factor 1 subunit beta; SL3/AKV core binding factor beta subunit; SL3/AKV core-binding factor beta subunit
Species
Homo sapiens (Human)
Source
E.coli
Expression Region
1-182aa
Target Protein Sequence
MPRVVPDQRSKFENEEFFRKLSRECEIKYTGFRDRPHEERQARFQNACRDGRSEIAFVATGTNLSLQFFPASWQGEQRQTPSREYVDLEREAGKVYLKAPMILNGVCVIWKGWIDLQRLDGMGCLEFDEERAQQEDALAQQAFEEARRRTREFEDRDRSHREEMEVRVSQLLAVTGKKTTRP
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight
37.5kDa
Protein Length
Full Length
Tag Info
N-terminal 6xHis-SUMO-tagged
Form
Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer
If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol.
Note: If you have any special requirement for the glycerol content, please remark when you place the order.
If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting and FAQs
Storage Condition
Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time
Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Notes
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA
Please contact us to get it.

Customer Reviews and Q&A

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Target Background

Function
Forms the heterodimeric complex core-binding factor (CBF) with RUNX family proteins (RUNX1, RUNX2, and RUNX3). RUNX members modulate the transcription of their target genes through recognizing the core consensus binding sequence 5'-TGTGGT-3', or very rarely, 5'-TGCGGT-3', within their regulatory regions via their runt domain, while CBFB is a non-DNA-binding regulatory subunit that allosterically enhances the sequence-specific DNA-binding capacity of RUNX. The heterodimers bind to the core site of a number of enhancers and promoters, including murine leukemia virus, polyomavirus enhancer, T-cell receptor enhancers, LCK, IL3 and GM-CSF promoters. CBF complexes repress ZBTB7B transcription factor during cytotoxic (CD8+) T cell development. They bind to RUNX-binding sequence within the ZBTB7B locus acting as transcriptional silencer and allowing for cytotoxic T cell differentiation.
Gene References into Functions
  1. This study investigated the role of circ-CBFB in chronic lymphocytic leukemia. The ID of circ-CBFB in circBase is hsa_circ_0000707, which locates at chromosome 16q22.1 and derived from the back-splicing of CBFB transcript. PMID: 29902450
  2. results suggest that CBFbeta-SMMHC has complex actions on human ribosome biogenesis at both the genomic and posttranscriptional level PMID: 28196984
  3. the presented study demonstrates that CBFB-MYH11-based MRD status during the first 3 months after allo-HCT, but not KIT mutations, can be used to identify patients with a high risk of relapse. PMID: 27650511
  4. discussion of the role of CBFB in diseases caused by their mutations or deletions (review) PMID: 28299663
  5. Both c-kit receptor (KIT) D816V and KIT N822K mutations underwent autophosphorylation in the absence of growth factor in leukemia TF-1 cell line. PMID: 28506695
  6. The co-existence of BCR-ABL1 and CBFB rearrangement is associated with poor outcome and a clinical course similar to that of CML-BP, and unlike de novo AML with CBFB rearrangement, suggesting that high-intensity chemotherapy with TKI should be considered in these patients. PMID: 28253536
  7. Moreover, using a CBF-beta loss-of-function mutant, the authors demonstrated that the interaction between CBF-beta and Vif was not sufficient for Vif assistance; a region including F68 in CBF-beta was also required for the stability and function of Vif. PMID: 28516844
  8. Vif stabilization by CBFbeta is mainly caused by impairing MDM2-mediated degradation. PMID: 27758855
  9. Mutational analysis of CBFbeta revealed that F68 and I55 residues are important and participate in a tripartite hydrophobic interaction with W5 of Vif to maintain a stable and functional Vif-CBFbeta complex. PMID: 28302150
  10. Our findings demonstrate that HSPCs exposed to non-cytotoxic levels of environmental chemicals and chemotherapeutic agents are prone to topoisomerase II-mediated DNA damage at the leukemia-associated genes MLL and CBFB. PMID: 26163765
  11. These results provide important information on the assembly of the Vif-CUL5-E3 ubiquitin ligase and identify a new viV binding interface with CBF-beta at the C-terminus of HIV-1 Vif. PMID: 25424878
  12. CBF-beta promoted steady-state levels of HIV-1 Vif by inhibiting the degradation of HIV-1 Vif through the proteasome pathway. PMID: 25582776
  13. CBFB contributes to the transcriptional regulation of ribosomal gene expression and provide further understanding of the epigenetic role of CBFB-SMMHC in proliferation and maintenance of the leukemic phenotype. PMID: 25079347
  14. we report a novel hypomethylation pattern, specific to CBFB-MYH11 fusion resulting from inv(16) rearrangement in acute myeloid leukemia the expression of which correlated with PBX3 differential methylation PMID: 25266220
  15. suggest that a different mechanism exists for the Vif-APOBEC interaction and that non-primates are not suitable animal models for exploring pharmacological interventions that disrupt Vif-CBF-beta interaction PMID: 25122780
  16. Suggest that CBFbeta retention in the midbody during cytokinesis reflects a novel function that contributes to epigenetic control. PMID: 24648201
  17. Transcriptional analysis revealed that upon fusion protein knockdown, a small subset of the CBFbeta-MYH11 target genes show increased expression, confirming a role in transcriptional repression PMID: 24002588
  18. Authors propose that CBFbeta acts as a chaperone to stabilize HIV-1 Vif during and after synthesis and to facilitate interaction of Vif with cellular cofactors required for the efficient degradation of APOBEC3G. PMID: 24522927
  19. In the absence of CBFbeta, Vif does not bind Cul5, thus preventing the assembly of the E3 ligase complex. PMID: 24390320
  20. CBF-beta is critical for the formation of the Vif-ElonginB/ElonginC-Cul5 core E3 ubiquitin ligase complex. PMID: 24390335
  21. Vif conserved residues E88/W89 are crucial for CBFbeta binding. PMID: 24418540
  22. data reveal the structural basis for Vif hijacking of the CBF-beta and CUL5 E3 ligase complex, laying a foundation for rational design of novel anti-HIV drugs PMID: 24402281
  23. This report of recurring FLT3 N676 mutations in core-binding factor (CBF) leukemias suggests a defined subgroup of CBF leukemias. PMID: 23878140
  24. We conclude that non-type A CBFB-MYH11 fusion types associate with distinct clinical and genetic features, including lack of KIT mutations, and a unique gene-expression profile in acute myeloid leukemia PMID: 23160462
  25. Our data indicate that the CBFbeta-SMMHC's C-terminus is essential to induce embryonic hematopoietic defects and leukemogenesis. PMID: 23152542
  26. A comparison of heat capacity changes supports a model in which CBFbeta prestabilizes Vif((1-192)) relative to Vif((95-192)) PMID: 23098073
  27. Vif proteins of human and simian immunodeficiency viruses require cellular CBFbeta to degrade APOBEC3G. PMID: 22205746
  28. Vif and CBF-beta physically interact, and that the amino-terminal region of Vif is required for this interaction PMID: 22190036
  29. CBF-beta is required for Vif-mediated degradation of APOBEC3G and therefore for preserving HIV-1 infectivity PMID: 22190037
  30. For routine clinical practice, it may be meaningful to screen for C-KIT mutations in AML1/ETO-positive patients, as well as for FLT3(D835) mutations in CBF-AML. PMID: 19603346
  31. The expression of Cbfbeta which were the key factors in osteogenic differentiation was also up-regulated. PMID: 20433876
  32. conclude that CBFbeta is required for a subset of Runx2-target genes that are sufficient to maintain the invasive phenotype of the cells PMID: 20591170
  33. Data collectively suggest that CBFbeta is required for malignant phenotype in prostate and ovarian cancer cells. PMID: 20607802
  34. has a role in hematopoiesis; preturbations result from expression of the leukemogenic fusion gene Cbfb-MYH11 PMID: 12239155
  35. Expression of CBFB is down regulated in a significant portion of gastric cancer cases; may be involved in gastric carcinogenesis PMID: 15386419
  36. Plag1 and Plagl2 are novel leukemia oncogenes that act by expanding hematopoietic progenitors expressing CbF beta-SMMHC. PMID: 15585652
  37. Detection of acute myeloid leukemic cells that are characterized by a CBFB-MYH11 gene fusion. PMID: 16502584
  38. These observations suggest that when abdominal GS is diagnosed, an analysis of the CBFB/MYH11 fusion gene is necessary to make an appropriate decision regarding treatment options, even if no chromosomal abnormalities are found. PMID: 16504290
  39. Agents interacting with the outer surface of the CBFbeta-SMMHC ACD that prevent multimerization may be effective as novel therapeutics in AML PMID: 16767164
  40. Rare fusion transcripts were correlated with an atypical cytomorphology not primarily suggestive for the FAB subtype acute myelocytic leukemia. PMID: 17287858
  41. Examine consequences of expression of abnormal chimeric protein CBFbeta-MYH11 in acute myelomonocytic leukemia. PMID: 17571080
  42. high CBFB protein level was an independent predictor of survival in colorectal cancer PMID: 19156145

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Involvement in disease
A chromosomal aberration involving CBFB is associated with acute myeloid leukemia of M4EO subtype. Pericentric inversion inv(16)(p13;q22). The inversion produces a fusion protein that consists of the 165 N-terminal residues of CBF-beta (PEPB2) with the tail region of MYH11.
Subcellular Location
Nucleus.
Protein Families
CBF-beta family
Database Links

HGNC: 1539

OMIM: 121360

KEGG: hsa:865

STRING: 9606.ENSP00000415151

UniGene: Hs.460988

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