SIRT7 Antibody [J3K9]

Catalog No.: F4019

    Application: Reactivity:

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    代表番号: 045-509-1970|電子メール:sales@selleck.co.jp

    使用情報

    Dilution
    1:1000
    1:30
    1:100
    Application
    WB, IP, IHC
    Source
    Rabbit Monoclonal Antibody
    Reactivity
    Mouse, Rat, Human
    Storage Buffer
    PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3
    Storage (from the date of receipt)
    -20°C (avoid freeze-thaw cycles), 2 years
    Predicted MW Observed MW
    44 kDa 45 kDa
    *なぜ予測分子量と実際の分子量が異なるのか?
    下記の原因により、実際の分子量が予測と異なる:タンパク質の翻訳後修飾(リン酸化/糖鎖付加),スプライシングバリアント,イソフォーム,相対的な電荷,ポリマー。

    Datasheet & SDS

    生物学的記述

    Specificity
    SIRT7 Antibody [J3K9] detects endogenous levels of total SIRT7 protein.
    Clone
    J3K9
    Synonym(s)
    SIR2L7; SIRT7; NAD-dependent protein deacetylase sirtuin-7; NAD-dependent protein deacylase sirtuin-7; Regulatory protein SIR2 homolog 7; SIR2-like protein 7
    Background
    SIRT7 is an NAD±dependent deacetylase and Class III HDAC from the conserved sirtuin family SIRT1-7, primarily found in the nucleolus and highly expressed in hematopoietic cells such as myeloid progenitors. SIRT7 is essential for rRNA processing, chromatin silencing, and cellular transformation. It includes a unique N-terminal three-helical domain α1-α3 with arginines R30, R37, R64, R68, and R74 that mediate nucleosome and DNA engagement across the acidic patch and gyres, a flexible linker or hinge helix α2, and a catalytic core featuring DNA-binding loops such as H217, R218, K272-276, R289, and R290. F239 secures H3K36 in the active site, conferring deacylation specificity over H3K18. SIRT7 is recruited by Elk-4 to promoters, where it deacetylates H3K18 to repress transcription, maintains ribosomal biogenesis via RNA polymerase I, and facilitates DNA repair by deacetylating ATM for dephosphorylation. It shifts between tightly gripping DNA when targeting H3K36 and a relaxed, bent linker conformation when targeting H3K18. Overexpression of SIRT7 leads to global reduction of H3K18 acetylation, driving anchorage-independent growth, low-serum survival, cell-cycle entry, escape from contact inhibition, and tumorigenesis in xenograft models, while knockout impairs these transformed phenotypes. In cancer, SIRT7 amplification in prostate, lung, kidney, and pancreas correlates with poor prognosis through H3K18 hypoacetylation, and SIRT7 also promotes leukemia and lymphoma via 17q25 alterations and supports E1A-induced transformation.
    References

    技術サポート

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