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Recombinant Human NADPH–cytochrome P450 reductase (POR), Truncated

Enhance your research endeavors with our high-quality Recombinant Human POR protein. Specifically tailored for the study of signal transduction, this NADPH--cytochrome P450 reductase (CPR; P450R) protein is produced in an E. coli expression system to ensure reliability and efficiency in your experiments. The partial protein (2-671aa) based on BC034277 reference sequence allows for outstanding performance in a variety of research applications. Equipped with an N-terminal GST-tag for effortless protein purification and detection, our Recombinant Human POR protein exhibits a purity greater than 90% as determined by SDS-PAGE. Available in both liquid and lyophilized powder forms, this premium protein provides flexibility and adaptability for your research needs. Choose our Recombinant Human POR protein for a dependable resource in the exploration of signal transduction pathways.

ACP02757

Enhance your research endeavors with our high-quality Recombinant Human POR protein. Specifically tailored for the study of signal transduction, this NADPH–cytochrome P450 reductase (CPR; P450R) protein is produced in an E. coli expression system to ensure reliability and efficiency in your experiments. The partial protein (2-671aa) based on BC034277 reference sequence allows for outstanding performance in a variety of research applications.
Equipped with an N-terminal GST-tag for effortless protein purification and detection, our Recombinant Human POR protein exhibits a purity greater than 90% as determined by SDS-PAGE. Available in both liquid and lyophilized powder forms, this premium protein provides flexibility and adaptability for your research needs. Choose our Recombinant Human POR protein for a dependable resource in the exploration of signal transduction pathways.

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Specifications


Cat.No ACP02757 Target NamePOR
FormLiquid or Lyophilized powderExpression SystemE.coli
Expression Range2-671aaMol Weight102.9kDa
Protein LengthPartial of BC034277PurityGreater than 90% as determined by SDS-PAGE.
Storage Buffer5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, Liquid form: default storage buffer is Tris/PBS-based buffer, pH 8.0.

Immunogen Information


Target SpeciesHumanUniprot IDP16435
Background Information
  • Uniprot Id

    P16435

  • Target Species

    Human

  • Target Name

    POR

  • Target Full Name

    NADPH--cytochrome P450 reductase

  • Target Function

    This enzyme is required for electron transfer from NADP to cytochrome P450 in microsomes. It can also provide electron transfer to heme oxygenase and cytochrome B5.

  • Target Involvement

    Antley-Bixler syndrome, with genital anomalies and disordered steroidogenesis (ABS1); Disordered steroidogenesis due to cytochrome P450 oxidoreductase deficiency (DISPORD)

  • Target Subcellular Location

    Endoplasmic reticulum membrane; Single-pass membrane protein; Cytoplasmic side.

  • Target Protein Families

    NADPH--cytochrome P450 reductase family; Flavodoxin family; Flavoprotein pyridine nucleotide cytochrome reductase family

  • Target Synonyms

    CPR; CYPOR; Cytochrome p450 oxidoreductase; DKFZp686G04235; FLJ26468; NADPH Cytochrome P450 Reductase; NADPH dependent cytochrome P450 reductase; NADPH--cytochrome P450 reductase; NCPR_HUMAN; P450 (cytochrome) oxidoreductase; P450 Cytochrome Oxidoreductase; P450R; por

  • Target Background

    This gene encodes an endoplasmic reticulum membrane oxidoreductase that is essential for multiple metabolic processes, including reactions catalyzed by cytochrome P450 proteins for metabolism of steroid hormones, drugs and xenobiotics. The encoded protein has a flavin adenine dinucleotide (FAD)-binding domain and a flavodoxin-like domain which bind two cofactors, FAD and FMN, that allow it to donate electrons directly from NADPH to all microsomal P450 enzymes. Mutations in this gene cause a complex set of disorders, including apparent combined P450C17 and P450C21 deficiency, amenorrhea and disordered steroidogenesis, congenital adrenal hyperplasia and Antley-Bixler syndrome, that resemble those caused by defects in steroid metabolizing enzymes such as aromatase, 21-hydroxylase, and 17 alpha-hydroxylase.

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