目录号 | 产品详情 | 靶点 | |
---|---|---|---|
T16432 | MAPK Ras | ||
Pan-RAS-IN-1是一种广谱的 Ras 抑制剂。Pan-RAS-IN-1破坏 Ras 蛋白及其作用子的相互作用。 | |||
T5469 | Raf Ras | ||
K-Ras-IN-1 是K-Ras 抑制剂。K-Ras-IN-1 能与 K-Ras (WT)、K-Ras (G12D)、K-Ras (G12V) 和 H-Ras 结合。它对胰腺癌、结肠癌和肺癌的具潜在的研究价值。 | |||
T37422L | Ras | ||
Ras Inhibitory Peptide acetate 是一种参与 Ras 依赖性信号通路的肽,Ras 在致癌受体引发的人类癌症中起重要作用。 | |||
T11738 | Ras | ||
K-Ras G12C-IN-4 是一种 KRAS G12C 共价抑制剂。 | |||
T6556 | Raf | ||
K-Ras(G12C) inhibitor 9 是致癌 K-Ras(G12C) 的变构抑制剂。 | |||
T3725 | Raf | ||
KRas(G12C) inhibitor 6 是一种变构的,选择性的 K-Ras(G12C)抑制剂。 | |||
T6555 | Apoptosis Raf Ras | ||
K-Ras(G12C) inhibitor 12是一种K-Ras(G12C)抑制剂,作用于H1792细胞,EC50为0.32 μM。 | |||
T8659 | PDE | ||
K-Ras-PDEδ-IN-1 是新型的 K-Ras-PDEδ 抑制剂,它能够以低纳摩尔Kd8 nM 与 PDEδ 的法尼基结合袋竞争性结合。 | |||
T12692 | Others | ||
RAS GTPase inhibitor 1 is a inhibitor of RAS GTPase, with anti-tumor activity. | |||
T36642 | |||
RAS/RAS-RAF-IN-1 is a potent RAS and RAS-RAF inhibitor. RAS/RAS-RAF-IN-1 has a KD of 5.0 μμ-15 μμ for cyclophilin A (CYPA) binding affinity. RAS/RAS-RAF-IN-1 has antitumor activity[1]. RAS/RAS-RAF-IN-1 (compound 89; for 4 hours) has an EC50 of 0.5 μμ-5.0 μμ for BRAF-GTP-KRAS-G12C disruption and has an IC50 of 1.0 μμ-10 μμ for pERK inhibition in H358 cells[1]. [1]. Meizhong Jin, et al. Compounds that participate in cooperative binding and uses thereof. WO2020132597A1. |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
---|---|---|---|---|---|
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
|
|||||
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
|
|||||
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
|
|||||
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
|
|||||
TMPJ-00510 | KRAS Protein, Human, Recombinant (G12C, His) | Human | E. coli | ||
K-Ras belongs to the small GTPase superfamily, Ras family. As 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. Ras proteins bind GDP/GTP and possess intrinsic GTPase activity. Plays an important role in the regulation of cell proliferation. Plays a role in promoting oncogenic events by inducing transcriptional silencing of tumor suppressor genes (TSGs) in colorectal cancer (CRC) cells in a ZNF304-dependent manner. 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 have been found to be associated with Noonan syndrome[4] and cardio-facio-cutaneous syndrome. Somatic K-Ras mutations are found at high rates in Leukemias, colon cancer, pancreatic cancer and lung cancer.
|
|||||
TMPJ-00511 | KRAS Protein, Human, Recombinant (G12V, His) | Human | E. coli | ||
K-Ras belongs to the small GTPase superfamily, Ras family. As 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. Ras proteins bind GDP/GTP and possess intrinsic GTPase activity. Plays an important role in the regulation of cell proliferation. Plays a role in promoting oncogenic events by inducing transcriptional silencing of tumor suppressor genes (TSGs) in colorectal cancer (CRC) cells in a ZNF304-dependent manner. 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 have been found to be associated with Noonan syndrome[4] and cardio-facio-cutaneous syndrome. Somatic K-Ras mutations are found at high rates in Leukemias, colon cancer, pancreatic cancer and lung cancer.
|
|||||
TMPY-04203 | RAB1B Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
RAB1B, a member of the RAS oncogene family, was significantly down-regulated in highly metastatic breast cancer cells. Moreover, down-regulation of RAB1B was also found to promote the proliferation and migration of TNBC cells in vitro and in vivo. Mechanistically, loss of RAB1B resulted in elevated expression of TGF-beta receptor 1 (TbetaR1) through decreased degradation of ubiquitin, increased levels of phosphorylated SMAD3 and TGF-beta-induced epithelial-mesenchymal transition (EMT). Furthermore, low RAB1B expression correlated with poor prognosis in breast cancer patients.RAB1B acts as a metastasis suppressor in TNBC by regulating the TGF-beta/SMAD signaling pathway and RAB1B may serve as a novel biomarker of prognosis and the response to anti-tumor therapeutics for patients with TNBC.
|
|||||
TMPY-03487 | NRAS Protein, Human, Recombinant (His) | Human | E. coli | ||
NRAS was discovered by researchers at the Institute of Cancer Research, funded by the Cancer Research Campaign (now Cancer Research UK). NRAS gene is a member of the Ras gene family. It is mapped on chromosome 1, and it is activated in HL6, a promyelocytic leukemia line. The mammalian ras gene family consists of the Harvey and Kirsten ras genes (HRAS and KRAS), an inactive pseudogene of each (c-Hras2 and c-Kras1), and the N-ras gene. They differ significantly only in the C-terminal 4 amino acids. These ras genes have GTP/GDP binding and GTPase activity, and their normal function may be as G-like regulatory proteins involved in the normal control of cell growth. The NRAS gene specifies two main transcripts of 2Kb and 4.3Kb. The difference between the two transcripts is a simple extension through the termination site of the 2Kb transcript. The NRAS gene consists of seven exons (-I, I, II, III, IV, V, VI).Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy
|
|||||
TMPY-04152 | RAB7A Protein, Rat, Recombinant (His) | Rat | E. coli | ||
RAB7A is a ubiquitous small GTPase, which controls transport to late endocytic compartments. Silencing or overexpression of wild type RAB7A changed the soluble/insoluble rate of peripherin indicating that RAB7A is important for peripherin organization and function. Besides, disease-causing RAB7A mutant proteins bind more strongly to peripherin and their expression causes a significant increase in the amount of soluble peripherin. The altered interaction between disease-causing RAB7A mutants and peripherin could play an important role in CMT2B neuropathy.
|
|||||
TMPY-04112 | RAB31 Protein, Human, Recombinant (His) | Human | E. coli | ||
RAB31 Protein, Human, Recombinant (His) is expressed in E. coli with His tag. The predicted molecular weight is 23.9 kDa. Accession number: Q13636
|
|||||
TMPY-04059 | RAB27B Protein, Human, Recombinant | Human | HEK293 | ||
RAB27B is a member of the Rab family GTPases involved in vesicle trafficking. The Rab27 subfamily consists of Rab27a and Rab27b. The human RAB27B gene is organized in six exons, spanning about 69 kb in the chromosome 18q21.1 region. The Rab27 subfamily of Ras-like GTPases is highly conserved in mammals. There is high degree of conservation in sequence and gene structure between RAB27A and RAB27B genes. Exogenous expression of Rab27b in melanocytes results in melanosomal association as observed for Rab27a, suggesting the two Rab27 proteins are functional homologues. As with RAB27A in Griscelli Disease, RAB27B may be also associated with human disease mapping to chromosome 18.
|
|||||
TMPY-04026 | RAB27B Protein, Human, Recombinant (mFc) | Human | HEK293 | ||
RAB27B is a member of the Rab family GTPases involved in vesicle trafficking. The Rab27 subfamily consists of Rab27a and Rab27b. The human RAB27B gene is organized in six exons, spanning about 69 kb in the chromosome 18q21.1 region. The Rab27 subfamily of Ras-like GTPases is highly conserved in mammals. There is high degree of conservation in sequence and gene structure between RAB27A and RAB27B genes. Exogenous expression of Rab27b in melanocytes results in melanosomal association as observed for Rab27a, suggesting the two Rab27 proteins are functional homologues. As with RAB27A in Griscelli Disease, RAB27B may be also associated with human disease mapping to chromosome 18.
|
|||||
TMPY-04311 | RAB11B Protein, Human, Recombinant (His) | Human | HEK293 | ||
The two recurrent dominant mutations in RAB11B leading to a neurodevelopmental syndrome, likely caused by altered GDP/GTP binding that inactivate the protein and induce GEF binding and protein mislocalization.
|
|||||
TMPY-03430 | RheB Protein, Human, Recombinant (His) | Human | Baculovirus-Insect Cells | ||
RHEB is a recently discovered member of the Ras superfamily that may be involved in neural plasticity. This function is novel and not typically associated with the Ras proteins. RHEB gene is a member of the small GTPase superfamily and encodes a lipid-anchored, cell membrane protein with five repeats of the RAS-related GTP-binding region. RHEB is vital in regulation of growth and cell cycle progression due to its role in the insulin / TOR / S6K signaling pathway. The protein has GTPase activity and shuttles between a GDP-bound form and a GTP-bound form, and farnesylation of RHEB is required for this activity. Three pseudogenes have been mapped, two on chromosome 1 and one on chromosome 22.
|
|||||
TMPY-00490 | RAB6A Protein, Human, Recombinant (His) | Human | E. coli | ||
Rab6 is one of the most conserved Rab GTPaes throughout evolution and the most abundant Rab protein associated with the Golgi complex. The two ubiquitous Rab isoforms, Rab6A and Rab6A', that are generated by alternative splicing of the RAB6A gene, regulate several transport steps at the Golgi level, including retrograde transport between endosomes and Golgi, anterograde transport between Golgi and the plasma membrane, and intra-Golgi and Golgi to endoplasmic reticulum transport. In MEF cells, most of the functions were attributed to the two ubiquitous Rab6 isoforms.
|
|||||
TMPY-03813 | RAB27B Protein, Human, Recombinant (His) | Human | HEK293 | ||
RAB27B is a member of the Rab family GTPases involved in vesicle trafficking. The Rab27 subfamily consists of Rab27a and Rab27b. The human RAB27B gene is organized in six exons, spanning about 69 kb in the chromosome 18q21.1 region. The Rab27 subfamily of Ras-like GTPases is highly conserved in mammals. There is high degree of conservation in sequence and gene structure between RAB27A and RAB27B genes. Exogenous expression of Rab27b in melanocytes results in melanosomal association as observed for Rab27a, suggesting the two Rab27 proteins are functional homologues. As with RAB27A in Griscelli Disease, RAB27B may be also associated with human disease mapping to chromosome 18.
|
|||||
TMPY-00610 | RAB2 Protein, Mouse, Recombinant (His) | Mouse | E. coli | ||
RAB2A, a protein essential for ER-to-Golgi transport, is critical in promoting proteolytic activity and 3D invasiveness of breast cancer (BC) cell lines.RAB2A is amplified and elevated in human BC and is a powerful and independent predictor of disease recurrence in BC patients. Thus, RAB2A is a novel trafficking determinant essential for regulation of a mesenchymal invasive program of BC dissemination. At the cellular levels, RAB2A controls both canonical polarized Golgi-to-Plasma membrane trafficking of the junctional protein E-cadherin, and post-endocytic trafficking of the membrane-bound metalloprotease, MT1-MMP.
|
|||||
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.
|
|||||
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.
|
|||||
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.
|
|||||
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.
|
|||||
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.
|
|||||
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.
|
|||||
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.
|
|||||
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.
|
|||||
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.
|
|||||
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.
|
|||||
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.
|
|||||
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.
|
|||||
TMPK-01405 | HLA-A*11:01&B2M&KRAS G12V (VVVGAVGVGK) 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.
|
|||||
TMPK-01443 | HLA-A*11:01&B2M&KRAS G12V (VVVGAVGVGK) 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. The virtual screening approach to discover novel KRAS inhibitors and synthetic lethality interactors of KRAS are discussed in detail.
|
|||||
TMPK-01450 | HLA-C*03:04&B2M&KRAS G12D (GADGVGKSAL) 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.
|
|||||
TMPK-01460 | HLA-A*11:01&B2M&KRAS G12S (VVVGASGVGK) 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.
|
|||||
TMPK-01511 | HLA-A*03:01&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.
|
|||||
TMPK-01428 | HLA-A*11:01&B2M&KRAS G12D (VVGADGVGK) Monomer Protein, Human, MHC (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.
|
|||||
TMPK-01462 | HLA-A*11:01&B2M&KRAS G12C (VVVGACGVGK) 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.
|
|||||
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.
|
|||||
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.
|
|||||
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.
|
|||||
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.
|
|||||
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.
|
|||||
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.
|
|||||
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.
|
|||||
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.
|
|||||
TMPK-01432 | HLA-A*11:01&B2M&KRAS G12A (VVVGAAGVGK) 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.
|
|||||
TMPK-01507 | HLA-A*11:01&B2M&KRAS G12D (VVVGADGVGK) 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.
|
|||||
TMPK-01512 | HLA-A*03:01&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.
|
|||||
TMPK-01402 | HLA-A*11:01&B2M&KRAS G12V (VVGAVGVGK) 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.
|
|||||
TMPK-01430 | HLA-A*11:01&B2M&KRAS G12D (VVVGADGVGK) 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.
|
|||||
TMPK-01456 | HLA-C*03:04&B2M&KRAS G12D (GADGVGKSAL) 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.
|