Mouse B- And T-Lymphocyte Attenuator (BTLA) Protein

Product specifications

Proteins and Peptides

B- And T-Lymphocyte Attenuator (BTLA)

E. coli

Mouse

Unconjugated

Molecular Weight: Calculated MW: 21.2 kDa
Concentration: Prior to lyophilization: 200 µg/ml
Sequence Fragment: Glu30-Tyr183
Tag: N-terminal His tag

Recombinant

> 90%

10 µg

50 µg

100 µg

200 µg

500 µg

Lyophilized To keep the original salt concentration, we recommend reconstituting to the original concentration prior to lyophilization (see Concentration) in ddH2O. If a lower concentration is required, dilute in PBS, pH 7.4. If a higher concentration is required, the product can be reconstituted directly in PBS, pH 7.4, though please note that this will change the overall salt concentration. The stock concentration should be between 0.1-1.0 mg/ml. Do not vortex.

WB, SDS-PAGE

Prior to lyophilization: PBS, pH 7.4, containing 0.01% Sarcosyl, 1 mM DTT, 5% Trehalose and Proclin-300.

Shipped within 5-7 working days.

Store at 2-8 °C for up to one month. Store at -80 °C for up to one year. Avoid repeated freeze/thaw cycles.

No

Q7TSA3

B- and T-lymphocyte attenuator,BTLA1,CD272,

Protein BTLA

RUO

This product is for research use only.   Not for human consumption, cosmetic, therapeutic or diagnostic use.

Descripción

B and T Lymphocyte Attenuator (BTLA) is an immunoglobulin superfamily receptor expressed on various immune cells, notably B cells, T cells, macrophages, and dendritic cells. BTLA is a crucial immune checkpoint molecule that modulates immune responses by interacting with its ligand, Herpesvirus entry mediator (HVEM), to maintain immune homeostasis and prevent overactivation that could lead to autoimmune responses. As an immune checkpoint, BTLA is part of a larger family of inhibitory receptors, such as PD-1 and CTLA-4, that regulate immune cell activity to mitigate excessive inflammatory responses. However, BTLA has distinct binding affinities and structural features, which influence its role in modulating immune responses, inflammation, and tolerance. BTLA's interaction with HVEM is unique among immune checkpoint pathways because HVEM also binds several other ligands, including LIGHT (TNFSF14) and lymphotoxin α. This interaction allows for complex regulatory functions, enabling BTLA to provide inhibitory signals that dampen T cell receptor (TCR) and B cell receptor (BCR) signaling. Such regulation is vital in preventing autoimmunity and controlling immune responses in infection, inflammation, and cancer, where immune modulation can prevent tumor growth but also, if dysregulated, may suppress necessary immune responses against cancer cells.

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