Cell Line

CysLT1 (Cysteinyl leukotriene receptor 1) is previous named as LTD4 receptor (leukotriene D4 receptor). It is a receptor for cysteinyl leukotrienes and has highest affinity to leukotriene D4 (LTD4). The receptor mediates contraction and proliferation of smooth muscle, edema, eosinophil migration and damage to the mucus layer in the lung caused by LTD4. A CysLT1 selective antagonist, montelukast, is used clinically in the treatment of asthma.. This response is mediated via a G-protein that activates a phosphatidylinositol-calcium second messenger system. The rank order of affinities for the leukotrienes is LTD4 >> LTE4 = LTC4 >> LTB4.

Lysophosphatidic acid (LPA), a bioactive lipid produced by several cell types including postmitotic neurons and activated platelets, is thought to be involved in various biological processes, including brain development. Three cognate G-protein coupled receptors encoded by lpa(1)/lp(A1)/Edg-2/Gpcr26, lpa(2)/lp(A2)/Edg-4, and lpa(3)/lp(A3)/Edg-7 mediate the cellular effects of LPA. However, many LPA-induced responses, including phospholipase C activation, Ca²⁺ mobilization, adenylyl cyclase activation, proliferation, JNK activation, AKT activation, and stress fiber formation, were absent or severely reduced in embryonic fibroblasts derived from lpa(1)(-/-) lpa(2)(-/-) mice. The lysophosphatidic acid receptor LPA2 or endothelial differentiation, G-protein coupled receptor 4(EDG-4) is expressed most abundantly in testes and peripheral blood leukocytes. It is reported to be a distinctive functional marker for ovarian carcinoma.

Extracellular adenosine mediates a multitude of biological effects, including wakefulness, antiarrythmia, bronchoconstriction and response to ischemia and oxidative stress. A family of four G-protein coupled adrenoceptors, A1, A2A, A2B and A3, is responsible for these effects. A3, which couples to G_i/o, is expressed in a wide range of human tissues, but most predominantly in the lung and liver. Recent animal model studies have shown that A3 receptors play important roles in brain ischemia, immunosuppresion, and bronchospasm. A3 receptor agonists and/or agonists may have important clinical value in the treatment of asthma and inflammation. Mice lacking A3 receptors display reduced mast cell degranulation and bronchoconstriction in response to adenosine.

Somatostatin acts at many sites to inhibit the release of many hormones and other secretory proteins. The biologic effects of somatostatin are probably mediated by a family of G protein-coupled receptors that are expressed in a tissue-specific manner. SST1 receptor is a Gi/Go-coupled GPCR which is expressed in pancreatic islets, pituitary, Cerebellum (Purkinje cells), frontal cortex (pyramidal cells), hippocampus (CA1-4 subfields and some granule cells of the dentate gyrus). It inhibits cAMP accumulation and stimulates tyrosine phosphatase activity, it also can antiproliferation.<br>GenScript's SST1-expressing stable cell line was made in CHO-K1/Gqi5 host cell and optimized for calcium assays.

Gastric inhibitory polypeptide receptor (GIPR) is a Gs-coupled GPCR which is expressed in the pancreas, stomach, small intestine, adipose tissue, adrenal cortex, pituitary, heart, testis, endothelial cells, bone, trachea, spleen, thymus, lung, kidney, thyroid, and several regions in the CNS. Its ligand GIP is secreted after meal ingestion has been shown to stimulate bone formation resulting in lower occurrences of osteoporosis. GIPR may have therapeutic potential in the treatment of type 2 diabetes and obesity.

Programmed cell death protein 1, also known as PD-1 and CD279 (cluster of differentiation 279), is a protein that in humans is encoded by the PDCD1 gene. PD-1, functioning as an immune checkpoint, plays an important role in down regulating the immune system by preventing the activation of T-cells, which in turn reduces autoimmunity and promotes self-tolerance. The inhibitory effect of PD-1 is accomplished through a dual mechanism of promoting apoptosis (programmed cell death) in antigen specific T-cells in lymph nodes while simultaneously reducing apoptosis in regulatory T cells (suppressor T cells).

CTLA4 or CTLA-4 (cytotoxic T-lymphocyte-associated protein 4), also known as CD152 (cluster of differentiation 152), is a protein receptor that functions as an immune checkpoint and downregulates immune responses. CTLA4 is constitutively expressed in regulatory T cells but only upregulated in conventional T cells after activation – a phenomenon which is particularly notable in cancers. It acts as an "off" switch when bound to CD80 or CD86 on the surface of antigen-presenting cells.<br/> The CTLA-4 protein is encoded by the Ctla4 gene in mice and the CTLA4 gene in humans.

T cell immunoglobulin mucin-3 (TIM-3) is a member of the T-cell Immunoglobulin- and Mucin-domain-containing family of type I membrane glycoproteins that regulate autoimmune and allergic disease. TIM-3 is selectively expressed on Th1 cells and interacts with galectin-9. It negatively regulates Th1 responses and affects macrophage activation. The 280 amino acid mature human TIM-3 contains a V-type Ig-like domain that shows multiple polymorphisms, followed by a mucin-like domain in the 171 amino acid extracellular region, which shares 60% amino acid identity with mouse TIM-3 ECD.

Lymphocyte-activation gene 3, also known as LAG-3, is a protein which in humans is encoded by the LAG3 gene.[1] LAG3, which was discovered in 1990[2] and was designated CD223 (cluster of differentiation 223) after the Seventh Human Leucocyte Differentiation Antigen Workshop in 2000[3]. LAG-3 is a cell surface molecule with diverse biologic effects on T cell function. It is an immune checkpoint receptor and as such is the target of various drug development programs by pharmaceutical companies seeking to develop new treatments for cancer and autoimmune disorders.