目录号 | 产品详情 | 靶点 | |
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T61585 | |||
Sulindac (sodium) (MK-231) 是一种非甾体抗炎剂,具有口服活性。Sulindac (sodium) 用于减轻疼痛,肿胀和关节僵硬的关节炎。Sulindac 还用于脊柱关节炎、痛风性关节炎的研究。Sulindac (sodium) 作为一种免疫调节剂,可通过阻断 NF-κB 信号通路下调 PD-L1,调节 pMMR CRC 对抗 PD-L1 免疫治疗的应答,抑制结直肠癌 CRC 的发生发展。 Sulindac 还可通过下调 SIRT1 抑制 TGF-β1-诱导的 EMT,抑制肺癌细胞的迁移和侵袭。 | |||
T0459 | COX Autophagy | ||
Sulindac (Sulindac sulfoxide) 是一种非甾体类抗炎剂,可抑制COX-2的活性,也可抑制 COX-2 的过表达。它是一种亚磺酰基茚衍生物前药,具有潜在的抗肿瘤活性。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-00500 | Latent TGF beta 1 Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
TGF-beta 1 is a member of the transforming growth factor beta (TGF-beta) family. The transforming growth factor-beta family of polypeptides are involved in the regulation of cellular processes, including cell division, differentiation, motility, adhesion and death. TGF-beta 1 positively and negatively regulates many other growth factors. It inhibits the secretion and activity of many other cytokines including interferon-γ, tumor necrosis factor-alpha and various interleukins. It can also decrease the expression levels of cytokine receptors. Meanwhile, TGF-beta 1 also increases the expression of certain cytokines in T cells and promotes their proliferation, particularly if the cells are immature. TGF-beta 1 also inhibits proliferation and stimulates apoptosis of B cells, and plays a role in controlling the expression of antibody, transferrin and MHC class II proteins on immature and mature B cells. As for myeloid cells, TGF-beta 1can inhibit their proliferation and prevent their production of reactive oxygen and nitrogen intermediates. However, as with other cell types, TGF-beta 1 also has the opposite effect on cells of myeloid origin. TGF-beta 1 is a multifunctional protein that controls proliferation, differentiation and other functions in many cell types. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts. Once cells lose their sensitivity to TGF-beta1-mediated growth inhibition, autocrine TGF-beta signaling can promote tumorigenesis. Elevated levels of TGF-beta1 are often observed in advanced carcinomas, and have been correlated with increased tumor invasiveness and disease progression.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-01133 | Latent TGF beta 1 Protein, Human, Recombinant (His) | Human | HEK293 | ||
TGF-beta 1 is a member of the transforming growth factor beta (TGF-beta) family. The transforming growth factor-beta family of polypeptides are involved in the regulation of cellular processes, including cell division, differentiation, motility, adhesion and death. TGF-beta 1 positively and negatively regulates many other growth factors. It inhibits the secretion and activity of many other cytokines including interferon-γ, tumor necrosis factor-alpha and various interleukins. It can also decrease the expression levels of cytokine receptors. Meanwhile, TGF-beta 1 also increases the expression of certain cytokines in T cells and promotes their proliferation, particularly if the cells are immature. TGF-beta 1 also inhibits proliferation and stimulates apoptosis of B cells, and plays a role in controlling the expression of antibody, transferrin and MHC class II proteins on immature and mature B cells. As for myeloid cells, TGF-beta 1can inhibit their proliferation and prevent their production of reactive oxygen and nitrogen intermediates. However, as with other cell types, TGF-beta 1 also has the opposite effect on cells of myeloid origin. TGF-beta 1 is a multifunctional protein that controls proliferation, differentiation and other functions in many cell types. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts. Once cells lose their sensitivity to TGF-beta1-mediated growth inhibition, autocrine TGF-beta signaling can promote tumorigenesis. Elevated levels of TGF-beta1 are often observed in advanced carcinomas, and have been correlated with increased tumor invasiveness and disease progression.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-04211 | Latent TGF beta 1 Protein, Cynomolgus, Recombinant (His) | Cynomolgus | HEK293 | ||
TGF-beta 1 is a member of the transforming growth factor beta (TGF-beta) family. The transforming growth factor-beta family of polypeptides are involved in the regulation of cellular processes, including cell division, differentiation, motility, adhesion and death. TGF-beta 1 positively and negatively regulates many other growth factors. It inhibits the secretion and activity of many other cytokines including interferon-γ, tumor necrosis factor-alpha and various interleukins. It can also decrease the expression levels of cytokine receptors. Meanwhile, TGF-beta 1 also increases the expression of certain cytokines in T cells and promotes their proliferation, particularly if the cells are immature. TGF-beta 1 also inhibits proliferation and stimulates apoptosis of B cells, and plays a role in controlling the expression of antibody, transferrin and MHC class II proteins on immature and mature B cells. As for myeloid cells, TGF-beta 1can inhibit their proliferation and prevent their production of reactive oxygen and nitrogen intermediates. However, as with other cell types, TGF-beta 1 also has the opposite effect on cells of myeloid origin. TGF-beta 1 is a multifunctional protein that controls proliferation, differentiation and other functions in many cell types. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts. Once cells lose their sensitivity to TGF-beta1-mediated growth inhibition, autocrine TGF-beta signaling can promote tumorigenesis. Elevated levels of TGF-beta1 are often observed in advanced carcinomas, and have been correlated with increased tumor invasiveness and disease progression.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-00608 | TGF beta 1 Protein, Rat/Mouse, Recombinant | Mouse,Rat | HEK293 | ||
TGF-beta 1 is a member of the transforming growth factor beta (TGF-beta) family. The transforming growth factor-beta family of polypeptides are involved in the regulation of cellular processes, including cell division, differentiation, motility, adhesion and death. TGF-beta 1 positively and negatively regulates many other growth factors. It inhibits the secretion and activity of many other cytokines including interferon-γ, tumor necrosis factor-alpha and various interleukins. It can also decrease the expression levels of cytokine receptors. Meanwhile, TGF-beta 1 also increases the expression of certain cytokines in T cells and promotes their proliferation, particularly if the cells are immature. TGF-beta 1 also inhibits proliferation and stimulates apoptosis of B cells, and plays a role in controlling the expression of antibody, transferrin and MHC class II proteins on immature and mature B cells. As for myeloid cells, TGF-beta 1can inhibit their proliferation and prevent their production of reactive oxygen and nitrogen intermediates. However, as with other cell types, TGF-beta 1 also has the opposite effect on cells of myeloid origin. TGF-beta 1 is a multifunctional protein that controls proliferation, differentiation and other functions in many cell types. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts. Once cells lose their sensitivity to TGF-beta1-mediated growth inhibition, autocrine TGF-beta signaling can promote tumorigenesis. Elevated levels of TGF-beta1 are often observed in advanced carcinomas, and have been correlated with increased tumor invasiveness and disease progression.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-02638 | TGF beta 1 Protein, Human/Rhesus/Cynomolgus/Canine, Recombinant | Human,Rhesus,Cynomolgus,Canine | CHO | ||
TGF-beta 1 is a member of the transforming growth factor beta (TGF-beta) family. The transforming growth factor-beta family of polypeptides are involved in the regulation of cellular processes, including cell division, differentiation, motility, adhesion and death. TGF-beta 1 positively and negatively regulates many other growth factors. It inhibits the secretion and activity of many other cytokines including interferon-γ, tumor necrosis factor-alpha and various interleukins. It can also decrease the expression levels of cytokine receptors. Meanwhile, TGF-beta 1 also increases the expression of certain cytokines in T cells and promotes their proliferation, particularly if the cells are immature. TGF-beta 1 also inhibits proliferation and stimulates apoptosis of B cells, and plays a role in controlling the expression of antibody, transferrin and MHC class II proteins on immature and mature B cells. As for myeloid cells, TGF-beta 1can inhibit their proliferation and prevent their production of reactive oxygen and nitrogen intermediates. However, as with other cell types, TGF-beta 1 also has the opposite effect on cells of myeloid origin. TGF-beta 1 is a multifunctional protein that controls proliferation, differentiation and other functions in many cell types. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts. Once cells lose their sensitivity to TGF-beta1-mediated growth inhibition, autocrine TGF-beta signaling can promote tumorigenesis. Elevated levels of TGF-beta1 are often observed in advanced carcinomas, and have been correlated with increased tumor invasiveness and disease progression.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPJ-00249 | TGF beta 1 Protein, Human, Recombinant (Avi), Biotinylated | Human | Human Cells | ||
Transforming Growth Factor β-1 (TGFβ-1) is a secreted protein which belongs to the TGF-β family. TGFβ-1 is abundantly expressed in bone, articular cartilage and chondrocytes and is increased in osteoarthritis (OA). TGFβ-1 performs many cellular functions, including the control of cell growth, cell proliferation, cell differentiation and apoptosis. The precursor is cleaved into a latency-associated peptide (LAP) and a mature TGFβ-1 peptide. TGFβ-1 may also form heterodimers with other TGFβ family members. It has been found that TGFβ-1 is frequently upregulated in tumor cells. Mutations in this gene results in Camurati-Engelmann disease.
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TMPY-03945 | Latent TGF beta 1 Protein, Rat, Recombinant (His) | Rat | HEK293 | ||
TGF-beta 1 is a member of the transforming growth factor beta (TGF-beta) family. The transforming growth factor-beta family of polypeptides are involved in the regulation of cellular processes, including cell division, differentiation, motility, adhesion and death. TGF-beta 1 positively and negatively regulates many other growth factors. It inhibits the secretion and activity of many other cytokines including interferon-γ, tumor necrosis factor-alpha and various interleukins. It can also decrease the expression levels of cytokine receptors. Meanwhile, TGF-beta 1 also increases the expression of certain cytokines in T cells and promotes their proliferation, particularly if the cells are immature. TGF-beta 1 also inhibits proliferation and stimulates apoptosis of B cells, and plays a role in controlling the expression of antibody, transferrin and MHC class II proteins on immature and mature B cells. As for myeloid cells, TGF-beta 1can inhibit their proliferation and prevent their production of reactive oxygen and nitrogen intermediates. However, as with other cell types, TGF-beta 1 also has the opposite effect on cells of myeloid origin. TGF-beta 1 is a multifunctional protein that controls proliferation, differentiation and other functions in many cell types. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts. Once cells lose their sensitivity to TGF-beta1-mediated growth inhibition, autocrine TGF-beta signaling can promote tumorigenesis. Elevated levels of TGF-beta1 are often observed in advanced carcinomas, and have been correlated with increased tumor invasiveness and disease progression.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-06355 | Latent TGF beta 1 & GARP Heterotrimer Protein, Human, Recombinant (His) | Human | HEK293 | ||
Latent TGF beta 1 & GARP Heterotrimer Protein, Human, Recombinant (His) is expressed in HEK293 with His tag. The predicted molecular weight is 108.72 kDa. Accession number: P01137
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TMPY-05521 | Latent TGF beta 1 Protein, Human, Recombinant (His), Biotinylated | Human | HEK293 | ||
TGF-beta 1 is a member of the transforming growth factor beta (TGF-beta) family. The transforming growth factor-beta family of polypeptides are involved in the regulation of cellular processes, including cell division, differentiation, motility, adhesion and death. TGF-beta 1 positively and negatively regulates many other growth factors. It inhibits the secretion and activity of many other cytokines including interferon-γ, tumor necrosis factor-alpha and various interleukins. It can also decrease the expression levels of cytokine receptors. Meanwhile, TGF-beta 1 also increases the expression of certain cytokines in T cells and promotes their proliferation, particularly if the cells are immature. TGF-beta 1 also inhibits proliferation and stimulates apoptosis of B cells, and plays a role in controlling the expression of antibody, transferrin and MHC class II proteins on immature and mature B cells. As for myeloid cells, TGF-beta 1can inhibit their proliferation and prevent their production of reactive oxygen and nitrogen intermediates. However, as with other cell types, TGF-beta 1 also has the opposite effect on cells of myeloid origin. TGF-beta 1 is a multifunctional protein that controls proliferation, differentiation and other functions in many cell types. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts. Once cells lose their sensitivity to TGF-beta1-mediated growth inhibition, autocrine TGF-beta signaling can promote tumorigenesis. Elevated levels of TGF-beta1 are often observed in advanced carcinomas, and have been correlated with increased tumor invasiveness and disease progression.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-05313 | Latent TGF beta 1 Protein, Mouse, Recombinant (His), Biotinylated | Mouse | HEK293 | ||
TGF-beta 1 is a member of the transforming growth factor beta (TGF-beta) family. The transforming growth factor-beta family of polypeptides are involved in the regulation of cellular processes, including cell division, differentiation, motility, adhesion and death. TGF-beta 1 positively and negatively regulates many other growth factors. It inhibits the secretion and activity of many other cytokines including interferon-γ, tumor necrosis factor-alpha and various interleukins. It can also decrease the expression levels of cytokine receptors. Meanwhile, TGF-beta 1 also increases the expression of certain cytokines in T cells and promotes their proliferation, particularly if the cells are immature. TGF-beta 1 also inhibits proliferation and stimulates apoptosis of B cells, and plays a role in controlling the expression of antibody, transferrin and MHC class II proteins on immature and mature B cells. As for myeloid cells, TGF-beta 1can inhibit their proliferation and prevent their production of reactive oxygen and nitrogen intermediates. However, as with other cell types, TGF-beta 1 also has the opposite effect on cells of myeloid origin. TGF-beta 1 is a multifunctional protein that controls proliferation, differentiation and other functions in many cell types. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts. Once cells lose their sensitivity to TGF-beta1-mediated growth inhibition, autocrine TGF-beta signaling can promote tumorigenesis. Elevated levels of TGF-beta1 are often observed in advanced carcinomas, and have been correlated with increased tumor invasiveness and disease progression.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPJ-00771 | TGF beta 1 Protein, Mouse/Rat, Recombinant | Mouse,Rat | Human Cells | ||
Transforming growth factor beta 1 (TGFβ1) is the prototype of a growing superfamily of peptide growth factors and plays a prominent role in a variety of cellular processes, including cell-cycle progression, cell differentiation, reproductive function, development, motility, adhesion, neuronal growth, bone morphogenesis, wound healing, and immune surveillance. TGF-β1, TGF-β2 and TGF-β3 signal via the same heteromeric receptor complex, consisting of a ligand binding TGF-β receptor type II (TβR-II), and a TGF-β receptor type I (TβR-I). Signal transduction from the receptor to the nucleus is mediated via SMADs. TGF-β expression is found in cartilage, bone, teeth, muscle, heart, blood vessels, haematopoitic cells, lung, kidney, gut, liver, eye, ear, skin, and the nervous system.
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TMPY-00229 | Latent TGF beta 1 Protein, Canine, Recombinant (His) | Canine | HEK293 | ||
TGF-beta 1 is a member of the transforming growth factor beta (TGF-beta) family. The transforming growth factor-beta family of polypeptides are involved in the regulation of cellular processes, including cell division, differentiation, motility, adhesion and death. TGF-beta 1 positively and negatively regulates many other growth factors. It inhibits the secretion and activity of many other cytokines including interferon-γ, tumor necrosis factor-alpha and various interleukins. It can also decrease the expression levels of cytokine receptors. Meanwhile, TGF-beta 1 also increases the expression of certain cytokines in T cells and promotes their proliferation, particularly if the cells are immature. TGF-beta 1 also inhibits proliferation and stimulates apoptosis of B cells, and plays a role in controlling the expression of antibody, transferrin and MHC class II proteins on immature and mature B cells. As for myeloid cells, TGF-beta 1can inhibit their proliferation and prevent their production of reactive oxygen and nitrogen intermediates. However, as with other cell types, TGF-beta 1 also has the opposite effect on cells of myeloid origin. TGF-beta 1 is a multifunctional protein that controls proliferation, differentiation and other functions in many cell types. It plays an important role in bone remodeling as it is a potent stimulator of osteoblastic bone formation, causing chemotaxis, proliferation and differentiation in committed osteoblasts. Once cells lose their sensitivity to TGF-beta1-mediated growth inhibition, autocrine TGF-beta signaling can promote tumorigenesis. Elevated levels of TGF-beta1 are often observed in advanced carcinomas, and have been correlated with increased tumor invasiveness and disease progression.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPJ-00250 | LAP (TGF-beta 1) Protein, Human, Recombinant (His & Avi), Biotinylated | Human | Human Cells | ||
Transforming growth factor beta (TGFβ) family members are secreted in inactive complexes with a latency-associated peptide (LAP), a protein derived from the N-terminal region of the TGFβ gene product. Extracellular activation of these complexes is a critical step in regulation of TGFβ function in vivo. The TGFβ1 LAP is a ligand for the integrin αvβ6 and that αvβ6-expressing cells induce spatially restricted activition of TGFβ1. And LAP identifies a novel CD4+/CD25+ regulatory T cell subset with TGFbeta-mediated function and enhanced suppression of experimental autoimmune encephalomyelitis.
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TMPJ-00772 | Latent TGF-beta 1 Protein, Mouse, Recombinant (His & Avi), Biotinylated | Mouse | Human Cells | ||
Transforming growth factor beta (TGFβ) is a multifunctional cytokine that regulates cell growth, differentiation, adhesion, migration and death dependent on cell type, developmental stage, or tissue conditions. There are three isoforms of TGFβ (TGFβ-1, -2 and -3). latent TGF-β1 plays a protective role against bleomycin-induced lung inflammation and fibrosis. The inhibitory effect of latent TGF-β1 on lung inflammation and fibrosis may be associated with the counter-regulatory mechanism between latent and active TGF-β 1, the negative regulatory role of Smad7 in activation of both NF-κB and TGF-β/Smad signaling pathways, and importantly, the GARP-Foxp3 regulatory mechanism in rebalancing the Treg/Th17 response. Some studies have shown that TGFB1 (Cys33Ser) mice develop multiorgan inflammation and tumors consistent with reduced TGF-b1 activity.
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TMPJ-00622 | Latent TGF-beta 1 Protein, Cynomolgus, Recombinant (His) | Cynomolgus | Human Cells | ||
Transforming growth factor beta (TGFβ) is a multifunctional cytokine that regulates cell growth, differentiation, adhesion, migration and death dependent on cell type, developmental stage, or tissue conditions. There are three isoforms of TGFβ (TGFβ-1, -2 and -3). latent TGF-β1 plays a protective role against bleomycin-induced lung inflammation and fibrosis. The inhibitory effect of latent TGF-β1 on lung inflammation and fibrosis may be associated with the counter-regulatory mechanism between latent and active TGF-β 1, the negative regulatory role of Smad7 in activation of both NF-κB and TGF-β/Smad signaling pathways, and importantly, the GARP-Foxp3 regulatory mechanism in rebalancing the Treg/Th17 response. Some studies have shown that TGFB1 (Cys33Ser) mice develop multiorgan inflammation and tumors consistent with reduced TGF-b1 activity.
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TMPY-01384 | Endoglin/CD105 Protein, Human, Recombinant (His) | Human | HEK293 | ||
Endoglin, also known as CD105, is a type I homodimeric transmembrane glycoprotein with a large, disulfide-linked, extracellular region and a short, constitutively phosphorylated cytoplasmic tail. Endoglin contains an RGD tripeptide which is a key recognition structure in cellular adhesion,,suggesting a critical role for endoglin in the binding of endothelial cells to integrins and/or other RGD receptors. Endoglin is highly expressed on vascular endothelial cells, chondrocytes, and syncytiotrophoblasts of term placenta. It is also found on activated monocytes, mesenchymal stem cells and leukemic cells of lymphoid and myeloid lineages. As an accessory receptor for the TGF-β superfamily ligands, endoglin binds TGF-β1 and TGF-β3 with high affinity not by itself but by associating with TGF-β type II receptor (TβRII) and activates the downstream signal pathways. In addition, in human umbilical vein endothelial cells, ALK-1 is also a receptor kinase for endoglin threonine phosphorylation, and mutations in either of the two genes result in the autosomal-dominant vascular dysplasia, hereditary hemorrhagic telangiectasia (HHT). Endoglin has been regarded as a powerful biomarker of neovascularization, and is associated with several solid tumor types.
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TMPY-01870 | IL-9 Protein, Human, Recombinant (His) | Human | Baculovirus-Insect Cells | ||
Interleukin 9, also known as IL-9, is a cytokine (cell signaling molecule) belonging to the group of interleukins. IL-9 is a cytokine that acts as a regulator of a variety of hematopoietic cells. This cytokine stimulates cell proliferation and prevents apoptosis. It functions through the interleukin 9 receptor (IL-9R), which activates different signal transducer and activator (STAT) proteins and thus connects this cytokine to various biological processes. Genetic studies on a mouse model of asthma demonstrated that this cytokine is a determining factor in the pathogenesis of bronchial hyperresponsiveness. IL-9 is a key molecule that affects the differentiation of TH17 cells and Treg function. IL-9 predominantly produced by TH17 cells synergizes with TGF-β1 to differentiate naive CD4+ T cells into TH17 cells, while IL-9 secretion by TH17 cells is regulated by IL-23. Interestingly, IL-9 enhances the suppressive functions of FoxP3+ CD4+ Treg cells in vitro, and the absence of IL-9 signaling weakens the suppressive activity of nTregs in vivo, leading to an increase in effector cells and worsening of experimental autoimmune encephalomyelitis. The mechanism of IL-9 effects on TH17 and Tregs is through activation of STAT3 and STAT5 signaling. Our findings highlight the role of IL-9 as a regulator of pathogenic versus protective mechanisms of immune responses.
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TMPJ-00259 | TGF beta 2 Protein, Human, Recombinant (Avi), Biotinylated | Human | Human Cells | ||
Transforming growth factor beta (TGFβ) is a multifunctional cytokine that regulates cell growth, differentiation, adhesion, migration and death dependent on cell type, developmental stage, or tissue conditions. There are three isoforms of TGFβ (TGFβ-1, -2 and -3). TGFB2 could be a potential biomarker for screening, surveillance and prognosis in GC, and that TGFB2 might drive EMT in GC through the NGF/TrKs pathway. Overexpression of TGFB2 may drive EMT through the neuriterelated signaling and affect TMB levels by regulating the DNA damage repair pathways and immune infiltrates.TGF-β2 is an immune suppressor involvedin the development of immune tolerance, and recombinant TGF-β2 incubation is more potent than TGF-β1 or TGF-β3 incubation in suppressing macrophage inflammatory responses.
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TMPJ-00260 | Latent TGF-beta 2 Protein, Human, Recombinant (His & Avi), Biotinylated | Human | Human Cells | ||
Transforming growth factor beta (TGFβ) is a multifunctional cytokine that regulates cell growth, differentiation, adhesion, migration and death dependent on cell type, developmental stage, or tissue conditions. There are three isoforms of TGFβ (TGFβ-1, -2 and -3). TGFB2 could be a potential biomarker for screening, surveillance and prognosis in GC, and that TGFB2 might drive EMT in GC through the NGF/TrKs pathway. Overexpression of TGFB2 may drive EMT through the neuriterelated signaling and affect TMB levels by regulating the DNA damage repair pathways and immune infiltrates.TGF-β2 is an immune suppressor involvedin the development of immune tolerance, and recombinant TGF-β2 incubation is more potent than TGF-β1 or TGF-β3 incubation in suppressing macrophage inflammatory responses.
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TMPY-00783 | Endoglin/CD105 Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
Endoglin, also known as CD105, is a type I homodimeric transmembrane glycoprotein with a large, disulfide-linked, extracellular region and a short, constitutively phosphorylated cytoplasmic tail. Endoglin contains an RGD tripeptide which is a key recognition structure in cellular adhesion,,suggesting a critical role for endoglin in the binding of endothelial cells to integrins and/or other RGD receptors. Endoglin is highly expressed on vascular endothelial cells, chondrocytes, and syncytiotrophoblasts of term placenta. It is also found on activated monocytes, mesenchymal stem cells and leukemic cells of lymphoid and myeloid lineages. As an accessory receptor for the TGF-β superfamily ligands, endoglin binds TGF-β1 and TGF-β3 with high affinity not by itself but by associating with TGF-β type II receptor (TβRII) and activates the downstream signal pathways. In addition, in human umbilical vein endothelial cells, ALK-1 is also a receptor kinase for endoglin threonine phosphorylation, and mutations in either of the two genes result in the autosomal-dominant vascular dysplasia, hereditary hemorrhagic telangiectasia (HHT). Endoglin has been regarded as a powerful biomarker of neovascularization, and is associated with several solid tumor types.
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TMPY-01615 | Endoglin/CD105 Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
Endoglin, also known as CD105, is a type I homodimeric transmembrane glycoprotein with a large, disulfide-linked, extracellular region and a short, constitutively phosphorylated cytoplasmic tail. Endoglin contains an RGD tripeptide which is a key recognition structure in cellular adhesion,,suggesting a critical role for endoglin in the binding of endothelial cells to integrins and/or other RGD receptors. Endoglin is highly expressed on vascular endothelial cells, chondrocytes, and syncytiotrophoblasts of term placenta. It is also found on activated monocytes, mesenchymal stem cells and leukemic cells of lymphoid and myeloid lineages. As an accessory receptor for the TGF-β superfamily ligands, endoglin binds TGF-β1 and TGF-β3 with high affinity not by itself but by associating with TGF-β type II receptor (TβRII) and activates the downstream signal pathways. In addition, in human umbilical vein endothelial cells, ALK-1 is also a receptor kinase for endoglin threonine phosphorylation, and mutations in either of the two genes result in the autosomal-dominant vascular dysplasia, hereditary hemorrhagic telangiectasia (HHT). Endoglin has been regarded as a powerful biomarker of neovascularization, and is associated with several solid tumor types.
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TMPJ-00968 | NAMPT Protein, Human, Recombinant (His) | Human | E. coli | ||
Pre-B cell colony enhancing factor (PBEF) was originally identified as a cytokine that potentiated the clonal expansion and differentiation of pre-B cells, but it is also acknowledged to be the ubiquitous intracellular enzyme nicotinamide phosphoribosyltranferase (NAMPT) and the adipokine “visfatin”. PBEF is constitutively expressed in the fetal membranes where its greatest expression is in the amnion. It has intracellular and extracellular forms. Most of the intracellular functions of PBEF are due to its role as a Nampt which can induce angiogenesis through upregulation of VEGF and VEGFR and secretion of MCP-1. Extracellular PBEF has been shown to increase inflammatory cytokines, such as TNF-α, IL-1β, IL-16, and TGF-β1. PBEF also increases the production of IL-6, TNF-α, and IL-1β in CD14+ monocyctes, macrophages, and dendritic cells, enhances the effectiveness of T cells.
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TMPY-05221 | IL-9 Protein, Mouse, Recombinant (His) | Mouse | Baculovirus-Insect Cells | ||
Interleukin 9, also known as IL-9, is a cytokine (cell signaling molecule) belonging to the group of interleukins. IL-9 is a cytokine that acts as a regulator of a variety of hematopoietic cells. This cytokine stimulates cell proliferation and prevents apoptosis. It functions through the interleukin 9 receptor (IL-9R), which activates different signal transducer and activator (STAT) proteins and thus connects this cytokine to various biological processes. Genetic studies on a mouse model of asthma demonstrated that this cytokine is a determining factor in the pathogenesis of bronchial hyperresponsiveness. IL-9 is a key molecule that affects the differentiation of TH17 cells and Treg function. IL-9 predominantly produced by TH17 cells synergizes with TGF-β1 to differentiate naive CD4+ T cells into TH17 cells, while IL-9 secretion by TH17 cells is regulated by IL-23. Interestingly, IL-9 enhances the suppressive functions of FoxP3+ CD4+ Treg cells in vitro, and the absence of IL-9 signaling weakens the suppressive activity of nTregs in vivo, leading to an increase in effector cells and worsening of experimental autoimmune encephalomyelitis. The mechanism of IL-9 effects on TH17 and Tregs is through activation of STAT3 and STAT5 signaling. Our findings highlight the role of IL-9 as a regulator of pathogenic versus protective mechanisms of immune responses.
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TMPY-00459 | IL-9 Protein, Rat, Recombinant (His) | Rat | Baculovirus-Insect Cells | ||
Interleukin 9, also known as IL-9, is a cytokine (cell signaling molecule) belonging to the group of interleukins. IL-9 is a cytokine that acts as a regulator of a variety of hematopoietic cells. This cytokine stimulates cell proliferation and prevents apoptosis. It functions through the interleukin 9 receptor (IL-9R), which activates different signal transducer and activator (STAT) proteins and thus connects this cytokine to various biological processes. Genetic studies on a mouse model of asthma demonstrated that this cytokine is a determining factor in the pathogenesis of bronchial hyperresponsiveness. IL-9 is a key molecule that affects the differentiation of TH17 cells and Treg function. IL-9 predominantly produced by TH17 cells synergizes with TGF-β1 to differentiate naive CD4+ T cells into TH17 cells, while IL-9 secretion by TH17 cells is regulated by IL-23. Interestingly, IL-9 enhances the suppressive functions of FoxP3+ CD4+ Treg cells in vitro, and the absence of IL-9 signaling weakens the suppressive activity of nTregs in vivo, leading to an increase in effector cells and worsening of experimental autoimmune encephalomyelitis. The mechanism of IL-9 effects on TH17 and Tregs is through activation of STAT3 and STAT5 signaling. Our findings highlight the role of IL-9 as a regulator of pathogenic versus protective mechanisms of immune responses.
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