Render Target: SSR
Render Timestamp: 2024-10-10T23:07:03.455Z
Commit: 56767fe525c928647c8401233a175d0d607d385d
XML generation date: 2024-10-02 16:46:13.565
Product last modified at: 2024-10-03T07:00:54.897Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

KIF5B Antibody #18148

Filter:
  • WB

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 110
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    KIF5B Antibody recognizes endogenous levels of total KIF5B protein.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Lys32 of human KIF5B protein. Antibodies are purified by peptide affinity chromatography.

    Background

    Kinesin superfamily proteins (KIFs) are molecular motors that drive directional, microtubule-dependent intracellular transport of membrane-bound organelles and other macromolecules (e.g., proteins, nucleic acids). The intracellular transport functions of KIFs are fundamentally important for a variety of cellular functions, including mitotic and meiotic division, motility/migration, hormone and neurotransmitter release, and differentiation (1-4). Disruptions to KIF-mediated intracellular transport have been linked with a variety of pathologies, ranging from tumorigenesis to defects in higher order brain function such as learning and memory (4-6).

    KIF5 consists of three family members referred to as KIF5A, KIF5B, and KIF5C (7). KIF5A and KIF5C are specifically expressed in neurons whereas KIF5B is expressed ubiquitously (7-10). Targeted disruption of the kif5B gene resulted in embryonic lethality (11). These and other studies demonstrate that KIF5B plays an important role in the localization and distribution of major organelles, including the mitochondria and lysosome, and can contribute to autophagy (11-13). In addition, gene rearrangements involving KIF5B fusions to ALK and RET have been identified as drivers for lung cancer and other malignancies (14-18).
    1. Hirokawa, N. et al. (2009) Nat Rev Mol Cell Biol 10, 682-96.
    2. Yu, Y. and Feng, Y.M. (2010) Cancer 116, 5150-60.
    3. Park, J.J. et al. (2008) Mol Endocrinol 22, 989-1005.
    4. Hirokawa, N. et al. (2010) Neuron 68, 610-38.
    5. Yoshimura, Y. et al. (2010) Mol Cell Biol 30, 2206-19.
    6. Hirokawa, N. and Noda, Y. (2008) Physiol Rev 88, 1089-118.
    7. Nakagawa, T. et al. (1997) Proc Natl Acad Sci U S A 94, 9654-9.
    8. Aizawa, H. et al. (1992) J Cell Biol 119, 1287-96.
    9. Kanai, Y. et al. (2000) J Neurosci 20, 6374-84.
    10. Meng, Y.X. et al. (1997) Endocrinology 138, 1979-87.
    11. Tanaka, Y. et al. (1998) Cell 93, 1147-58.
    12. Cardoso, C.M. et al. (2009) PLoS One 4, e4424.
    13. Du, W. et al. (2016) Dev Cell 37, 326-36.
    14. Takeuchi, K. et al. (2009) Clin Cancer Res 15, 3143-9.
    15. Wong, D.W. et al. (2011) Cancer 117, 2709-18.
    16. Takeuchi, K. et al. (2012) Nat Med 18, 378-81.
    17. Ju, Y.S. et al. (2012) Genome Res 22, 436-45.
    18. Kohno, T. et al. (2012) Nat Med 18, 375-7.
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