CCL4 Protein, Human (P.pastoris, His)

CCL4 Protein, Human (P.pastoris, His) is a small cytokine of the CC chemokine subfamily that binds to the CCR5 chemokine receptor on the cell surface, promotes leukocyte aggregation under various inflammatory conditions, and contributes to immune protection against human immunodeficiency virus type 1. CCL4 Protein, Human (P.pastoris, His) is a recombinant human CCL4 (A24-Q92) expressed by P. pastoris with a His tag at the C-terminu^[1].

CCL4, also known as macrophage inflammatory protein (MIP-1β), belongs to the CC chemokine family and is a protein encoded in humans by the CCL4 gene, which belongs to the 17q11-q21 region of chromosome 17 and has a molecular weight of approximately 8-10 kDa. CCL4 can be produced by monocytes, B cells, T cells, NK cells, dendritic cells, neutrophils, fibroblasts, endothelial cells, and epithelial cells^[1]. CCL4 acts as a chemokine that binds to the G protein-coupled receptors CCR5 and CCR8 and acts as a chemoattractant for natural killer cells, monocytes and various other immune cells at sites of inflammation or damaged tissues. In parallel, CCL4 can also act as a major HIV suppressor produced by CD8+ T cells, inducing dose-dependent inhibition of different strains of HIV-1, HIV-2 and monkey immunodeficiency virus (SIV). Among them, the N-terminal processed form CCL4 (3-69), produced by proteolytic cleavage of peripheral blood lymphocytes after secretion, retains the ability to induce down-regulation of chemokine receptor CCR5 surface expression and inhibit CCR5-mediated HIV-1 entry into T cells^[2].

Human

P. pastoris

C-His

P13236 (A24-Q92)

6351  [NCBI]

12-16 kDa

Greater than 90% as determined by reducing SDS-PAGE.

<1 EU/μg, determined by LAL method.

• [1]. S G Irving, et al. Two inflammatory mediator cytokine genes are closely linked and variably amplified on chromosome 17q. Nucleic Acids Res. 1990 Jun 11;18(11):3261-70.  [Content Brief]

  [2]. Patricia Menten, et al. Macrophage inflammatory protein-1. Cytokine Growth Factor Rev. 2002 Dec;13(6):455-81.  [Content Brief]