目录号 | 产品详情 | 靶点 | |
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T24240 | Retinoid Receptor RAR/RXR | ||
K-8012 是 N 末端截短的 RXRα 的调节剂,并以 RXRα 依赖性方式提高抗癌活性。 | |||
T5S2309 | Others | ||
Hosenkoside K ((+)-Hosenkoside K) 是一种糖苷,分离自凤仙花种子。 | |||
T11742 | IL Receptor TNF | ||
K-7174 是一种新型细胞粘附抑制剂, 抑制由 IL-1β 或 TNF-α 诱导的血管细胞粘附分子 1 (VCAM-1) 的表达。 | |||
T8200 | AMPK Autophagy | ||
Ginkgolide K 是从银杏中分离得到的一种二萜类天然产物,有神经保护活性,可通过 AMPK/mTOR/ULK1信号通路诱导保护性自噬。 | |||
T15639 | PARP Wnt/beta-catenin | ||
K-756 是一种直接的 tankyrase(TNKS) 选择性抑制剂,对 TNKS1和 TNKS2的 ADP-核糖基化活性有抑制作用,IC50分别为 31 和 36 nM。 | |||
T19603 | Endogenous Metabolite | ||
Vitamin K (Kephton) 具有凝血作用,对凝血因子、基质-Gla 蛋白和骨钙素很重要。 | |||
T8936 | Others | ||
Proteinase K (proteinase K for tritirachium album) 是一种非特异性丝氨酸蛋白酶,可用于蛋白消化。它在有 SDS 或尿素存在的情况下,在很大 pH 值 (4-12)、盐浓度和温度单位内均有活性。 | |||
T3811 | P450 cell cycle arrest COX NO Synthase | ||
Ginsenoside C-K (Ginsenoside K) 是 Ginsenoside Rb1 的细菌代谢物,可通过抑制诱生型一氧化氮合酶和COX-2来发挥抗炎作用。它在人肝微粒体中抑制CYP2C9和CYP2A6活性,IC50分别为 32.0±3.6 和 63.6±4.2 μM。 | |||
T11733 | Acyltransferase | ||
K-604 dihydrochloride 是酰基辅酶 A:胆固醇酰基转移酶 1 的选择性抑制剂,IC50为 0.45±0.06 μM。 | |||
T9954 | Others | ||
K-975是一种高选择性的具有口服活性的TEAD 抑制剂,可有效抑制TEAD 和YAP1/TAZ 之间的蛋白质-蛋白质相互作用。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-04113 | KRAS Protein,Human,Recombinant(G12D & Q61H, His) | Human | E. coli | ||
K-Ras belongs to the small GTPase superfamily, Ras family. Like other members of the Ras family, K-Ras is a GTPase and is an early player in many signal transduction pathways. It is usually tethered to cell membranes because of the presence of an isoprenyl group on its C-terminus. K-Ras functions as a molecular on/off switch. Once it is turned on it recruits and activates proteins necessary for the propagation of growth factor and other receptors' signal, such as c-Raf and PI 3-kinase. It binds to GTP in the active state and possesses an intrinsic enzymatic activity that cleaves the terminal phosphate of the nucleotide converting it to GDP. Upon conversion of GTP to GDP, K-Ras is turned off. The rate of conversion is usually slow but can be sped up dramatically by an accessory protein of the GTPase activating protein class, for example, RasGAP. In turn, K-Ras can bind to proteins of the Guanine Nucleotide Exchange Factor class, for example, SOS1, which forces the release of bound nucleotide. Subsequently, K-Ras binds GTP present in the cytosol and the GEF is released from ras-GTP. Besides essential function in normal tissue signaling, the mutation of a K-Ras gene is an essential step in the development of many cancers. Several germline K-Ras mutations are associated with Noonan syndrome and Cardio-Facio-Cutaneous syndrome. Somatic K-Ras mutations are found at high rates in Leukemias, colon cancer, pancreatic cancer, and lung cancer.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-06056 | KRAS Protein, Human, Recombinant (G12D, His) | Human | E. coli | ||
K-Ras belongs to the small GTPase superfamily, Ras family. Like other members of the Ras family, K-Ras is a GTPase and is an early player in many signal transduction pathways. It is usually tethered to cell membranes because of the presence of an isoprenyl group on its C-terminus. K-Ras functions as a molecular on/off switch. Once it is turned on it recruits and activates proteins necessary for the propagation of growth factor and other receptors' signal, such as c-Raf and PI 3-kinase. It binds to GTP in the active state and possesses an intrinsic enzymatic activity that cleaves the terminal phosphate of the nucleotide converting it to GDP. Upon conversion of GTP to GDP, K-Ras is turned off. The rate of conversion is usually slow but can be sped up dramatically by an accessory protein of the GTPase activating protein class, for example, RasGAP. In turn, K-Ras can bind to proteins of the Guanine Nucleotide Exchange Factor class, for example, SOS1, which forces the release of bound nucleotide. Subsequently, K-Ras binds GTP present in the cytosol and the GEF is released from ras-GTP. Besides essential function in normal tissue signaling, the mutation of a K-Ras gene is an essential step in the development of many cancers. Several germline K-Ras mutations are associated with Noonan syndrome and Cardio-Facio-Cutaneous syndrome. Somatic K-Ras mutations are found at high rates in Leukemias, colon cancer, pancreatic cancer, and lung cancer.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-04116 | KRAS Protein,Human,Recombinant(G12C & Q61H, His) | Human | E. coli | ||
K-Ras belongs to the small GTPase superfamily, Ras family. Like other members of the Ras family, K-Ras is a GTPase and is an early player in many signal transduction pathways. It is usually tethered to cell membranes because of the presence of an isoprenyl group on its C-terminus. K-Ras functions as a molecular on/off switch. Once it is turned on it recruits and activates proteins necessary for the propagation of growth factor and other receptors' signal, such as c-Raf and PI 3-kinase. It binds to GTP in the active state and possesses an intrinsic enzymatic activity that cleaves the terminal phosphate of the nucleotide converting it to GDP. Upon conversion of GTP to GDP, K-Ras is turned off. The rate of conversion is usually slow but can be sped up dramatically by an accessory protein of the GTPase activating protein class, for example, RasGAP. In turn, K-Ras can bind to proteins of the Guanine Nucleotide Exchange Factor class, for example, SOS1, which forces the release of bound nucleotide. Subsequently, K-Ras binds GTP present in the cytosol and the GEF is released from ras-GTP. Besides essential function in normal tissue signaling, the mutation of a K-Ras gene is an essential step in the development of many cancers. Several germline K-Ras mutations are associated with Noonan syndrome and Cardio-Facio-Cutaneous syndrome. Somatic K-Ras mutations are found at high rates in Leukemias, colon cancer, pancreatic cancer, and lung cancer.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-01888 | KRAS Protein,Human, Recombinant (Q61H, His) | Human | E. coli | ||
K-Ras belongs to the small GTPase superfamily, Ras family. Like other members of the Ras family, K-Ras is a GTPase and is an early player in many signal transduction pathways. It is usually tethered to cell membranes because of the presence of an isoprenyl group on its C-terminus. K-Ras functions as a molecular on/off switch. Once it is turned on it recruits and activates proteins necessary for the propagation of growth factor and other receptors' signal, such as c-Raf and PI 3-kinase. It binds to GTP in the active state and possesses an intrinsic enzymatic activity that cleaves the terminal phosphate of the nucleotide converting it to GDP. Upon conversion of GTP to GDP, K-Ras is turned off. The rate of conversion is usually slow but can be sped up dramatically by an accessory protein of the GTPase activating protein class, for example, RasGAP. In turn, K-Ras can bind to proteins of the Guanine Nucleotide Exchange Factor class, for example, SOS1, which forces the release of bound nucleotide. Subsequently, K-Ras binds GTP present in the cytosol and the GEF is released from ras-GTP. Besides essential function in normal tissue signaling, the mutation of a K-Ras gene is an essential step in the development of many cancers. Several germline K-Ras mutations are associated with Noonan syndrome and Cardio-Facio-Cutaneous syndrome. Somatic K-Ras mutations are found at high rates in Leukemias, colon cancer, pancreatic cancer, and lung cancer.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-06567 | Granzyme K/GZMK Protein, Human, Recombinant (His) | Human | HEK293 | ||
Granzyme K/GZMK Protein, Human, Recombinant (His) is expressed in HEK293 with His tag. The predicted molecular weight is 27.56 kDa. Accession number: NP_002095.1
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TMPY-01050 | Cadherin 6/CDH6 Protein, Human, Recombinant (His) | Human | HEK293 | ||
Cadherins are a family of calcium-dependent, cell-cell adhesion molecules that play an important morpho regulatory role in a wide variety of tissues. Alterations in cadherin function have been implicated in tumor progression in a number of adenocarcinomas. Cadherin-6 (CDH6), also known as K-cadherin (KCAD), is a type-II classic cadherin cell-cell adhesion molecules, which are expressed in graded or areal patterns, as well as layer-specific patterns, in the cortical plate. Human Cadherin-6 is synthesized as a 790 aa type I transmembrane glycoprotein that contains an 18 aa signal peptide, a 35 aa propeptide, a 562 aa extracellular region, a 21 aa transmembrane segment, and a 154 aa cytoplasmic domain. There are five cadherin domains of approximately 110 aa each in the extracellular region. Cadherin-6 is highly expressed in brain, cerebellum, and kidney, and may contribute to the formation of the segmental structure of the early brain, as well as the development of renal proximal tubules. Weak expression is also detected lung, pancreas, and gastric mucosa. Additionally, it is specifically expressed in the proximal tubule of normal kidneys and in renal cell cancer. Thus, Cadherin-6 is a new prognostic factor for renal cancer.
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TMPH-03262 | Cathepsin K Protein, Rat, Recombinant (His) | Rat | E. coli | ||
Thiol protease involved in osteoclastic bone resorption and may participate partially in the disorder of bone remodeling. Displays potent endoprotease activity against fibrinogen at acid pH. May play an important role in extracellular matrix degradation. Involved in the release of thyroid hormone thyroxine (T4) by limited proteolysis of TG/thyroglobulin in the thyroid follicle lumen.
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TMPH-01061 | Cathepsin K Protein, Human, Recombinant (His) | Human | E. coli | ||
Thiol protease involved in osteoclastic bone resorption and may participate partially in the disorder of bone remodeling. Displays potent endoprotease activity against fibrinogen at acid pH. May play an important role in extracellular matrix degradation. Involved in the release of thyroid hormone thyroxine (T4) by limited proteolysis of TG/thyroglobulin in the thyroid follicle lumen.
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TMPH-02565 | Cathepsin K Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
Thiol protease involved in osteoclastic bone resorption. Displays potent endoprotease activity against fibrinogen at acid pH. May play an important role in extracellular matrix degradation. Involved in the release of thyroid hormone thyroxine (T4) by limited proteolysis of TG/thyroglobulin in the thyroid follicle lumen.
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TMPY-05004 | FGF-4 Protein, Human, Recombinant | Human | E. coli | ||
FGF (fibroblast growth factor) signalling is known to be required for many aspects of mesoderm formation and patterning during Xenopus development and has been implicated in regulating genes required for the specification of both blood and skeletal muscle lineages. Fibroblast growth factor 4 (FGF4) signaling induces differentiation from embryonic stem cells (ESCs) via the phosphorylation of downstream molecules such as mitogen-activated protein kinase/extracellular signal-related kinase (MEK) and extracellular signal-related kinase 1/2 (ERK1/2). Fibroblast Growth Factor 4 (FGF-4) could not only increase the proliferation of bone marrow mesenchymal stem cells (BMSCs), but also induce BMSCs into hepatocyte-like cells in vitro. FGF4 transduced BMSCs contributed to liver regeneration might by the transplanted microenvironment. The FGF4-bFGF BMSCs thus can enhance the survival of the transplanted cells, diminish myocardial fibrosis, promote myocardial angiogenesis, and improve cardiac functions.
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TMPY-05414 | NKG2D/CD314 Protein, Mouse, Recombinant (hFc) | Mouse | Baculovirus-Insect Cells | ||
KLRK1 (Killer Cell Lectin Like Receptor K1) is a Protein Coding gene. NKG2D, also known as CD314, is an immune receptor that consists of two disulfide-linked type II transmembrane proteins with short intracellular proteins incapable to transduce signals. To transduce signals, NKG2D needs adaptor proteins and it uses two adaptor proteins, DAP10 and DAP12. These two adaptor proteins associate as homodimers to NKG2D- therefore the entire receptor complex appears as a hexamer. NKG2D can send co-stimulatory signals to activate CD8 T cells. NKG2D also plays an important role in viral control. Cellular stress can induce ligands for NKG2D which results in the cell susceptible to NK cell-mediated lysis.
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TMPY-03376 | NKG2D/CD314 Protein, Rhesus, Recombinant (aa 78-216, His) | Rhesus | Baculovirus-Insect Cells | ||
KLRK1 (Killer Cell Lectin Like Receptor K1) is a Protein Coding gene. NKG2D, also known as CD314, is an immune receptor that consists of two disulfide-linked type II transmembrane proteins with short intracellular proteins incapable to transduce signals. To transduce signals, NKG2D needs adaptor proteins and it uses two adaptor proteins, DAP10 and DAP12. These two adaptor proteins associate as homodimers to NKG2D- therefore the entire receptor complex appears as a hexamer. NKG2D can send co-stimulatory signals to activate CD8 T cells. NKG2D also plays an important role in viral control. Cellular stress can induce ligands for NKG2D which results in the cell susceptible to NK cell-mediated lysis.
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TMPY-03256 | NKG2D/CD314 Protein, Human, Recombinant (aa 78-216, His) | Human | Baculovirus-Insect Cells | ||
KLRK1 (Killer Cell Lectin Like Receptor K1) is a Protein Coding gene. NKG2D, also known as CD314, is an immune receptor that consists of two disulfide-linked type II transmembrane proteins with short intracellular proteins incapable to transduce signals. To transduce signals, NKG2D needs adaptor proteins and it uses two adaptor proteins, DAP10 and DAP12. These two adaptor proteins associate as homodimers to NKG2D- therefore the entire receptor complex appears as a hexamer. NKG2D can send co-stimulatory signals to activate CD8 T cells. NKG2D also plays an important role in viral control. Cellular stress can induce ligands for NKG2D which results in the cell susceptible to NK cell-mediated lysis.
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TMPY-00467 | NKG2D/CD314 Protein, Human, Recombinant (hFc) | Human | CHO | ||
KLRK1 (Killer Cell Lectin Like Receptor K1) is a Protein Coding gene. NKG2D, also known as CD314, is an immune receptor that consists of two disulfide-linked type II transmembrane proteins with short intracellular proteins incapable to transduce signals. To transduce signals, NKG2D needs adaptor proteins and it uses two adaptor proteins, DAP10 and DAP12. These two adaptor proteins associate as homodimers to NKG2D- therefore the entire receptor complex appears as a hexamer. NKG2D can send co-stimulatory signals to activate CD8 T cells. NKG2D also plays an important role in viral control. Cellular stress can induce ligands for NKG2D which results in the cell susceptible to NK cell-mediated lysis.
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TMPY-00423 | FGFR2 Protein, Human, Recombinant (alpha IIIb, hFc) | Human | HEK293 | ||
FGFR2, also known as CD332, belongs to the fibroblast growth factor receptor subfamily where amino acid sequence is highly conserved between members and throughout evolution. FGFR2 acts as cell-surface receptor for fibroblast growth factors and plays an essential role in the regulation of cell proliferation, differentiation, migration and apoptosis, and in the regulation of embryonic development. It is required for normal embryonic patterning, trophoblast function, limb bud development, lung morphogenesis, osteogenesis and skin development. FGFR2 plays an essential role in the regulation of osteoblast differentiation, proliferation and apoptosis, and is required for normal skeleton development. It also promotes cell proliferation in keratinocytes and imature osteoblasts, but promotes apoptosis in differentiated osteoblasts. FGFR2 signaling is down-regulated by ubiquitination, internalization and degradation. Mutations that lead to constitutive kinase activation or impair normal CD332 maturation, internalization and degradation lead to aberrant signaling. Over-expressed FGFR2 promotes activation of STAT1. Defects in CD3322 are the cause of Crouzon syndrome, Jackson-Weiss syndrome, Apert syndrome, Pfeiffer syndrome, Beare-Stevenson cutis gyrata syndrome, familial scaphocephaly syndrome, lacrimo-auriculo-dento-digital syndrome and Antley-Bixler syndrome without genital anomalies or disordered steroidogenesis.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPY-00972 | FGFR2 Protein, Human, Recombinant (His & hFc) | Human | HEK293 | ||
FGFR2, also known as CD332, belongs to the fibroblast growth factor receptor subfamily where amino acid sequence is highly conserved between members and throughout evolution. FGFR2 acts as cell-surface receptor for fibroblast growth factors and plays an essential role in the regulation of cell proliferation, differentiation, migration and apoptosis, and in the regulation of embryonic development. It is required for normal embryonic patterning, trophoblast function, limb bud development, lung morphogenesis, osteogenesis and skin development. FGFR2 plays an essential role in the regulation of osteoblast differentiation, proliferation and apoptosis, and is required for normal skeleton development. It also promotes cell proliferation in keratinocytes and imature osteoblasts, but promotes apoptosis in differentiated osteoblasts. FGFR2 signaling is down-regulated by ubiquitination, internalization and degradation. Mutations that lead to constitutive kinase activation or impair normal CD332 maturation, internalization and degradation lead to aberrant signaling. Over-expressed FGFR2 promotes activation of STAT1. Defects in CD3322 are the cause of Crouzon syndrome, Jackson-Weiss syndrome, Apert syndrome, Pfeiffer syndrome, Beare-Stevenson cutis gyrata syndrome, familial scaphocephaly syndrome, lacrimo-auriculo-dento-digital syndrome and Antley-Bixler syndrome without genital anomalies or disordered steroidogenesis.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
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TMPK-01471 | HLA-A*11:01&B2M&KRAS WT (VVVGAGGVGK) Monomer Protein, Human, MHC (His & Avi), FITC-Labeled | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01439 | HLA-A*11:01&B2M&KRAS G12D (VVVGADGVGK) Tetramer Protein, Human, MHC (His & Avi), PE-Labeled | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01464 | HLA-A*11:01&B2M&KRAS G12R (VVVGARGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01490 | HLA-A*11:01&B2M&KRAS G12V (VVGAVGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01537 | HLA-A*11:01&B2M&KRAS G12D (VVVGADGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01457 | HLA-A*11:01&B2M&KRAS G12A (VVVGAAGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01431 | HLA-A*11:01&B2M&KRAS G12S (VVVGASGVGK) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01453 | HLA-A*03:01&B2M&KRAS G12V (VVVGAVGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01489 | HLA-A*11:01&B2M&KRAS WT (VVVGAGGVGK) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01400 | HLA-A*11:01&B2M&KRAS WT (VVVGAGGVGK) Monomer Protein, Human, MHC (E. coli, His & Avi), Biotinylated | Human | E. coli | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01536 | HLA-A*11:01&B2M&KRAS G12V (VVVGAVGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01407 | HLA-A*02:01&B2M&KRAS WT (KLVVVGAGGV) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | E. coli | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01526 | HLA-A*03:01&B2M&KRAS G12V (VVVGAVGVGK) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01458 | HLA-A*11:01&B2M&KRAS G12A (VVVGAAGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01463 | HLA-A*11:01&B2M&KRAS G12C (VVVGACGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01529 | HLA-A*11:01&B2M&KRAS G12D (VVVGADGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01408 | HLA-A*02:01&B2M&KRAS G12V (KLVVVGAVGV) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | E. coli | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01451 | HLA-C 03:04&B2M&KRAS G12D (GADGVGKSAL) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01401 | HLA-A*11:01&B2M&KRAS WT (VVVGAGGVGK) Monomer Protein, Human, MHC (E. coli, His & Avi) | Human | E. coli | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01429 | HLA-A*11:01&B2M&KRAS G12D (VVVGADGVGK) Monomer Protein, Human, MHC (E. coli, His & Avi), Biotinylated | Human | E. coli | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01488 | HLA-A*11:01&B2M&KRAS WT (VVVGAGGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01510 | HLA-A*03:01&B2M&KRAS WT (VVVGAGGVGK) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01433 | HLA-A*11:01&B2M&KRAS G12C (VVVGACGVGK) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01527 | HLA-A*03:01&B2M&KRAS G12V (VVVGAVGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01518 | HLA-A*11:01&B2M&KRAS G12V (VVVGAVGVGK) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-00596 | SECTM1 Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
SECTM1 is a T/NK cell "co-stimulatory" molecule that is expressed in the peripheral blood by neutrophils and monocytes.Human monocytic cells also displayed a pronounced negative regulation of SECTM1 mRNA expression by LPS, while at the protein level SECTM1 expression was also shown to be regulated by IFN and LPS. This tight regulation of SECTM1 gene expression and rapid upregulation highlights its relevance in the innate immune response.
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TMPK-01403 | HLA-A*11:01&B2M&KRAS G12V (VVGAVGVGK) Monomer Protein, Human, MHC (E. coli, His & Avi) | Human | E. coli | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01525 | HLA-A*11:01&B2M&KRAS G12V (VVGAVGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01427 | HLA-A*11:01&B2M&KRAS G12D (VVGADGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | E. coli | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01434 | HLA-A*11:01&B2M&KRAS G12R (VVVGARGVGK) Tetramer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01479 | HLA-A*11:01&B2M&KRAS WT (VVVGAGGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01461 | HLA-A*11:01&B2M&KRAS G12S (VVVGASGVGK) Monomer Protein, Human, MHC (His & Avi) | Human | HEK293 | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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TMPK-01399 | HLA-A*11:01&B2M&KRAS WT (VVGAGGVGK) Monomer Protein, Human, MHC (His & Avi), Biotinylated | Human | E. coli | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target.
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TMPK-01404 | HLA-A*11:01&B2M&KRAS G12V (VVVGAVGVGK) Monomer Protein, Human, MHC (E. coli, His & Avi), Biotinylated | Human | E. coli | ||
Kirsten rat sarcoma 2 viral oncogene homolog (KRAS) is the most commonly mutated oncogene in human cancer. The developments of many cancers depend on sustained expression and signaling of KRAS, which makes KRAS a high-priority therapeutic target. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
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