Anti-EKLF / KLF1 antibody (ab49158)


  • Product nameAnti-EKLF / KLF1 antibody
    See all EKLF / KLF1 primary antibodies
  • Description
    Rabbit polyclonal to EKLF / KLF1
  • Tested applicationsSuitable for: WB, ELISAmore details
  • Species reactivity
    Reacts with: Human
    Predicted to work with: Cow, Pig
  • Immunogen

    A region within synthetic peptide: QLFRGLQGPA PGPATSPSFL SCLGPGTVGT GLGGTAEDPG VIAETAPSKR, corresponding to internal sequence amino acids 217-266 of Human EKLF/ KLF1

  • Positive control
    • K562 cell lysate


Associated products


Our Abpromise guarantee covers the use of ab49158 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
WB Use a concentration of 2.5 µg/ml. Detects a band of approximately 38 kDa (predicted molecular weight: 38 kDa). Good results were obtained when blocked with 5% non-fat dry milk in 0.05% PBS-T.
ELISA Use at an assay dependent concentration.

ELISA titre using peptide based assay: 1:62500.


  • FunctionTranscription regulator of erythrocyte development that probably serves as a general switch factor during erythropoiesis. Is a dual regulator of fetal-to-adult globin switching. Binds to the CACCC box in the beta-globin gene promoter and acts as a preferential activator of this gene. Furthermore, it binds to the BCL11A promoter and activates expression of BCL11A, which in turn represses the HBG1 and HBG2 genes. This dual activity ensures that, in most adults, fetal hemoglobin levels are low. Able to activate CD44 and AQP1 promoters. When sumoylated, acts as a transcriptional repressor by promoting interaction with CDH2/MI2beta and also represses megakaryocytic differentiation.
  • Tissue specificityExpression restricted to adult bone marrow and fetal liver. Not expressed in myeloid nor lymphoid cell lines.
  • Involvement in diseaseDefects in KLF1 are the cause of congenital dyserythropoietic anemia type 4 (CDA4) [MIM:613673]. It is a blood disorder characterized by ineffective erythropoiesis and hemolysis resulting in anemia. Circulating erythroblasts and erythroblasts in the bone marrow show various morphologic abnormalities. Affected individuals with CDA4 also have increased levels of fetal hemoglobin.
  • Sequence similaritiesBelongs to the krueppel C2H2-type zinc-finger protein family.
    Contains 3 C2H2-type zinc fingers.
  • Post-translational
    Acetylated; can be acetylated on both Lys-274 and Lys-288. Acetylation on Lys-274 (by CBP) appears to be the major site affecting EKLF transactivation activity.
    Sumoylated; sumoylation, promoted by PIAS1, leads to repression of megakaryocyte differentiation. Also promotes the interaction with the CDH4 subunit of the NuRD repression complex.
    Phosphorylated primarily on serine residues in the transactivation domain. Phosphorylation on Thr-23 is critical for the transactivation activity.
  • Cellular localizationNucleus. Colocalizes with SUMO1 in nuclear speckles.
  • Information by UniProt
  • Database links
  • Alternative names
    • CDAN4 antibody
    • EKLF antibody
    • EKLF PEN antibody
    • Erythroid krueppel like transcription factor (EKLF) (Erythroid transcription factor) antibody
    • Erythroid krueppel-like transcription factor antibody
    • Erythroid Kruppel like factor antibody
    • Erythroid specific transcription factor EKLF antibody
    • HBFQTL6 antibody
    • Human erythroid-specific transcription factor EKLF mRNA complete cds antibody
    • INLU antibody
    • Klf1 antibody
    • KLF1_HUMAN antibody
    • Krueppel-like factor 1 antibody
    • Kruppel like factor 1 (erythroid) antibody
    see all

Anti-EKLF / KLF1 antibody images

  • Anti-EKLF / KLF1 antibody (ab49158) at 2.5 µg/ml + K562 cell lysate at 10 µg

    HRP conjugated anti-Rabbit IgG at 1/50,000 - 1/100,000 dilution

    Predicted band size : 38 kDa
    Observed band size : 38 kDa

References for Anti-EKLF / KLF1 antibody (ab49158)

ab49158 has not yet been referenced specifically in any publications.

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