TIM 1 Antibody [M14A22]

Catalog No.: F7934

    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
    1:2000
    1:100
    1:500
    Application
    WB, IP, IHC, IF, FCM
    Source
    Rabbit Monoclonal Antibody
    Reactivity
    Mouse
    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
    39 kDa 75 kDa,36 kDa, 20-250 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
    TIM 1 Antibody [M14A22] detects endogenous levels of total TIM 1 protein.
    Clone
    M14A22
    Synonym(s)
    CD365, Kim1, Tim1, Timd1, Havcr1, HAVcr-1, Kidney injury molecule 1, T cell immunoglobulin and mucin domain-containing protein 1, T cell membrane protein 1, T-cell immunoglobulin mucin receptor 1, KIM-1, TIMD-1, TIM-1
    Background
    TIM‑1 (T‑cell immunoglobulin and mucin domain‑1, HAVCR1) is a type I transmembrane receptor of the TIM family that is expressed on activated CD4⁺ T cells, B cells, invariant NKT cells, and some epithelial cells, where it regulates both adaptive and innate immune responses. The extracellular region contains an Ig‑like domain with a metal‑ion–dependent ligand‑binding site that recognizes phosphatidylserine on apoptotic cell membranes, followed by a heavily glycosylated mucin stalk, while the short cytoplasmic tail carries tyrosine and serine residues that connect TIM‑1 engagement to intracellular signaling cascades. Interaction of TIM‑1 with phosphatidylserine on apoptotic cells or with agonistic antibodies enhances CD4⁺ T‑cell activation, increases expression of Th2‑associated transcription factors, and promotes production of IL‑4, IL‑5, IL‑10, and IL‑13, linking TIM‑1 ligation to skewing of T‑helper differentiation toward Th2 profiles. TIM‑1 expression on T cells is upregulated under Th2‑skewing conditions, that TIM‑1 costimulation augments Th2 cytokine responses and airway eosinophilia, and that genetic or antibody‑mediated interference with TIM‑1 reduces Th2 cytokines and airway inflammation. TIM‑1 is also expressed on invariant NKT cells, where engagement in the presence of TCR stimulation enhances IL‑4 production and reduces IFN‑γ, adding a second route by which TIM‑1 biases effector programs toward type 2 immunity and contributes to airway hyperreactivity after recognition of apoptotic cells.
    References

    技術サポート

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