• Product nameAnti-PDE8B antibody
    See all PDE8B primary antibodies
  • Description
    Rabbit polyclonal to PDE8B
  • Tested applicationsSuitable for: WB, IPmore details
  • Species reactivity
    Reacts with: Human
    Predicted to work with: Horse, Guinea pig, Cow, Dog, Pig, Chimpanzee, Rhesus monkey, Gorilla, Orangutan
  • Immunogen

    Synthetic peptide, corresponding to a region within C terminal amino acids 835-885 of Human PDE8B (NP_003710.1)

  • Positive control
    • Whole cell lysate from HeLa cells.


  • FormLiquid
  • Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
  • Storage bufferPreservative: 0.09% Sodium azide
    Constituent: 99% Tris citrate/phosphate
    Note: pH 7 to 8.
  • Concentration information loading...
  • PurityImmunogen affinity purified
  • ClonalityPolyclonal
  • IsotypeIgG
  • Research areas

Associated products


Our Abpromise guarantee covers the use of ab112024 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 1/2000 - 1/10000. Predicted molecular weight: 99 kDa.
IP Use at 2-5 µg/mg of lysate.


  • FunctionHydrolyzes the second messenger cAMP, which is a key regulator of many important physiological processes. May be involved in specific signaling in the thyroid gland.
  • Tissue specificityAbundantly expressed in the thyroid. Also very weakly expressed in brain, spinal cord and placenta. In the thyroid isoform 1 predominates, and isoforms 2 and 6 are also highly expressed. In the placenta isoforms 1 and 2 are expressed equally. In the brain isoform 2 predominates.
  • PathwayPurine metabolism; 3',5'-cyclic AMP degradation; AMP from 3',5'-cyclic AMP: step 1/1.
  • Involvement in diseaseDefects in PDE8B are the cause of striatal degeneration autosomal dominant (ADSD) [MIM:609161]. It is a movement disorder affecting the striatal part of the basal ganglia and characterized by bradykinesia, dysarthria and muscle rigidity. These symptoms resemble idiopathic Parkinson disease, but tremor is not present.
  • Sequence similaritiesBelongs to the cyclic nucleotide phosphodiesterase family. PDE8 subfamily.
    Contains 1 PAS (PER-ARNT-SIM) domain.
  • DomainComposed of a C-terminal catalytic domain containing two putative divalent metal sites and an N-terminal regulatory domain.
  • Information by UniProt
  • Database links
  • Alternative names
    • 3' 5' cyclic nucleotide phosphodiesterase 8B antibody
    • 3'5' cyclic nucleotide phosphodiesterase 8B antibody
    • Cell proliferation-inducing gene 22 protein antibody
    • FLJ11212 antibody
    • High affinity cAMP specific and IBMX insensitive 3' 5' cyclic phosphodiesterase 8B antibody
    • High affinity cAMP specific and IBMX insensitive 3'5' cyclic phosphodiesterase 8B antibody
    • High affinity cAMP-specific and IBMX-insensitive 3',5'-cyclic phosphodiesterase 8B antibody
    • HSPDE 8B antibody
    • HsPDE8B antibody
    • PDE 8B antibody
    • PDE8B antibody
    • PDE8B_HUMAN antibody
    • Phosphodiesterase 8B antibody
    • Phosphodiesterase8B antibody
    • PIG22 antibody
    see all

Anti-PDE8B antibody images

  • Immunoprecipitation of PDE8B. Samples: Whole cell lysate from HeLa cells. 20% of IP loaded. Antibodies: Affinity purified rabbit anti-PDE8B antibody (ab112024) at 1 µg/ml. Lane 1- PDE8B was immunoprecipitated by rabbit anti-PDE8B antibody (ab112024) at 6 mcg/mg lysate. Lane 2- PDE8B was immunoprecipitated by an rabbit anti-PDE8B antibody that recognizes an upstream epitope. Lane 3- Rabbit IgG control. Detection: Chemiluminescence with exposure times of 3 minutes.
  • All lanes : Anti-PDE8B antibody (ab112024) at 0.4 µg/ml

    Lane 1 : Whole cell extracts from HeLa cells at 50 µg
    Lane 2 : Whole cell extracts from HeLa cells at 15 µg
    Lane 3 : Whole cell extracts from HeLa cells at 5 µg

    Predicted band size : 99 kDa

References for Anti-PDE8B antibody (ab112024)

ab112024 has not yet been referenced specifically in any publications.

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