KRAS Antibody (YA6861)
(Synonyms: c Ki ras2 antibody; c Kirsten ras protein antibody; c-K-ras antibody; c-Ki-ras antibody; Cellular c Ki ras2 proto oncogene antibody; Cellular transforming proto oncogene antibody; CFC2 antibody; cK Ras antibody; GTPase KRas antibody; K RAS p21 protein antibody; c Ki ras2 antibody; c Kirsten ras protein antibody)Based on 1 Customer Validation
KRAS Antibody (YA6861) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to KRAS.
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Host:
Mouse
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Isotype:
IgG
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Application:
WB, IHC-P, ICC/IF, FC
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Reactivity :
Human, Mouse, Rat
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Formulation:
Supplied in PBS (pH7.4), 0.1% BSA, 40% Glycerol. Preservative: 0.05% Sodium Azide.
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Conjugation:
Non-conjugated
Applications
| Application |
WB
WB: Western Blot
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
IHC-P
IHC-P: Immunohistochemistry-Paraffin
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FC
FC: Flow Cytometry
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| Dilution Ratio | 1:2000 | 1:100 | 1:1100 | 1:500-1:1000 |
Product Details
KRAS Antibody (YA6861) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to KRAS.
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Host Mouse
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Clonality Monoclonal
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Species ReactivityHuman, Mouse, Rat
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Observed Molecular WeightObserved band size: 22 kDaNote: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 22 kDa
SwissProt: P01116 Human ; P32883 Mouse ; P08644 Rat
Recombinant protein within human KRAS aa 2-186 (P01116-1).
affinity purified.
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS (pH7.4), 0.1% BSA, 40% Glycerol. Preservative: 0.05% Sodium Azide.
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Verification Images
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Western blot analysis of extracts from MCF-7(lane2(20μg), A431(lane3(20μg), A375(lane4(20μg) and C6(lane5(20μg) using KRAS Antibody (YA6861)(HY-P87170). Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST at 4°C overnight. The primary antibody (1/2000) and Loading control antibody (Beta Actin, HY-P80993, 1/10,000) was used in 5% non-fat milk in TBST for 2 hour at room temperature. Goat Anti-Mouse IgG-HRP Secondary Antibody (HY-P8004, 1/10,000) was used for 1 hour at room temperature.
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Immunohistochemical analysis of paraffin-embedded human Colon cancer tissue using KRAS antibody was performed. The section was pretreated using high-temperature and high-pressure mediated EDTA antigen retrieval buffer (pH 9.0), for 5 minutes. The tissues were incubated with primary antibody (HY-P87170, 1:1000 dilution) at room temperature for 60 minutes. Detection was performed using an HRP conjugated compact polymer system. DAB was used as the chromogen. The tissues were counterstained with hematoxylin and mounted with neutral balsam mounting medium.
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Immunohistochemical analysis of paraffin-embedded human Colon cancer tissue using KRAS antibody was performed. The section was pretreated using high-temperature and high-pressure mediated EDTA antigen retrieval buffer (pH 9.0), for 5 minutes. The tissues were incubated with primary antibody (HY-P87170, 1:1000 dilution) at room temperature for 60 minutes. Detection was performed using an HRP conjugated compact polymer system. DAB was used as the chromogen. The tissues were counterstained with hematoxylin and mounted with neutral balsam mounting medium.
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Immunohistochemical analysis of paraffin-embedded human Prostate Cancer tissue using KRAS antibody was performed. The section was pretreated using high-temperature and high-pressure mediated EDTA antigen retrieval buffer (pH 9.0), for 5 minutes. The tissues were incubated with primary antibody (HY-P87170, 1:1000 dilution) at room temperature for 60 minutes. Detection was performed using an HRP conjugated compact polymer system. DAB was used as the chromogen. The tissues were counterstained with hematoxylin and mounted with neutral balsam mounting medium.
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Immunohistochemical analysis of paraffin-embedded human Prostate Cancer tissue using KRAS antibody was performed. The section was pretreated using high-temperature and high-pressure mediated EDTA antigen retrieval buffer (pH 9.0), for 5 minutes. The tissues were incubated with primary antibody (HY-P87170, 1:1000 dilution) at room temperature for 60 minutes. Detection was performed using an HRP conjugated compact polymer system. DAB was used as the chromogen. The tissues were counterstained with hematoxylin and mounted with neutral balsam mounting medium.
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Immunohistochemical analysis of paraffin-embedded human Esophageal Carcinoma tissue using KRAS antibody was performed. The section was pretreated using high-temperature and high-pressure mediated EDTA antigen retrieval buffer (pH 9.0), for 5 minutes. The tissues were incubated with primary antibody (HY-P87170, 1:1000 dilution) at room temperature for 60 minutes. Detection was performed using an HRP conjugated compact polymer system. DAB was used as the chromogen. The tissues were counterstained with hematoxylin and mounted with neutral balsam mounting medium.
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Immunohistochemical analysis of paraffin-embedded human cholangiocarcinoma tissue using KRAS antibody was performed. The section was pretreated using high-temperature and high-pressure mediated EDTA antigen retrieval buffer (pH 9.0), for 5 minutes. The tissues were incubated with primary antibody (HY-P87170, 1:1000 dilution) at room temperature for 60 minutes. Detection was performed using an HRP conjugated compact polymer system. DAB was used as the chromogen. The tissues were counterstained with hematoxylin and mounted with neutral balsam mounting medium.
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Tyramide signaling amplification based immunofluorescence was performed on paraffin-embedded human Colon cancer tissue using KRAS antibody. Antigen retrieval was performed in EDTA buffer pH 9.0 (95 °C, 20 min) followed by cooling to RT. Then incubated with primary antibody (HY-P87170, 1:1000 dilution) at room temperature for 60 minutes and HRP conjugated secondary antibody for 10 minutes. Fluorescence was then developed with Vari Fluor 532 TSA (200×)(HY-D1832). The tissues were counterstained with DAPI and mounted with Anti-fade mounting medium.
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Tyramide signaling amplification based immunofluorescence was performed on paraffin-embedded human Colon cancer tissue using KRAS antibody. Antigen retrieval was performed in EDTA buffer pH 9.0 (95 °C, 20 min) followed by cooling to RT. Then incubated with primary antibody (HY-P87170, 1:1000 dilution) at room temperature for 60 minutes and HRP conjugated secondary antibody for 10 minutes. Fluorescence was then developed with Vari Fluor 532 TSA (200×)(HY-D1832). The tissues were counterstained with DAPI and mounted with Anti-fade mounting medium.
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Tyramide signaling amplification based immunofluorescence was performed on paraffin-embedded human Colon cancer tissue using KRAS antibody. Antigen retrieval was performed in EDTA buffer pH 9.0 (95 °C, 20 min) followed by cooling to RT. Then incubated with primary antibody (HY-P87170, 1:1000 dilution) at room temperature for 60 minutes and HRP conjugated secondary antibody for 10 minutes. Fluorescence was then developed with Vari Fluor 532 TSA (200×)(HY-D1832). The tissues were counterstained with DAPI and mounted with Anti-fade mounting medium.
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Tyramide signaling amplification based immunofluorescence was performed on paraffin-embedded human Prostate Cancer tissue using KRAS antibody. Antigen retrieval was performed in EDTA buffer pH 9.0 (95 °C, 20 min) followed by cooling to RT. Then incubated with primary antibody (HY-P87170, 1:1000 dilution) at room temperature for 60 minutes and HRP conjugated secondary antibody for 10 minutes. Fluorescence was then developed with Vari Fluor 532 TSA (200×)(HY-D1832). The tissues were counterstained with DAPI and mounted with Anti-fade mounting medium.
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Tyramide signaling amplification based immunofluorescence was performed on paraffin-embedded human Prostate Cancer tissue using KRAS antibody. Antigen retrieval was performed in EDTA buffer pH 9.0 (95 °C, 20 min) followed by cooling to RT. Then incubated with primary antibody (HY-P87170, 1:1000 dilution) at room temperature for 60 minutes and HRP conjugated secondary antibody for 10 minutes. Fluorescence was then developed with Vari Fluor 532 TSA (200×)(HY-D1832). The tissues were counterstained with DAPI and mounted with Anti-fade mounting medium.
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Tyramide signaling amplification based immunofluorescence was performed on paraffin-embedded human Prostate Cancer tissue using KRAS antibody. Antigen retrieval was performed in EDTA buffer pH 9.0 (95 °C, 20 min) followed by cooling to RT. Then incubated with primary antibody (HY-P87170, 1:1000 dilution) at room temperature for 60 minutes and HRP conjugated secondary antibody for 10 minutes. Fluorescence was then developed with Vari Fluor 532 TSA (200×)(HY-D1832). The tissues were counterstained with DAPI and mounted with Anti-fade mounting medium.
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Flow cytometric analysis of 1X106 HeLa cells labeling KRAS Antibody(HY-P87170, red). Cells were fixed with 4% paraformaldehyde and permeabilised with 90% methanol. Then stained with the primary antibody at 1/500 dilution for an hour at 4℃. AF488-conjugated Goat Anti-Mouse IgG H&L (HY-P8005) was used as the secondary antibody at 1/1,000 dilution for 30 minutes at 4℃. Mouse IgG Isotype Control (HY-P80757, blue) was used as the isotype control, cells without incubation with primary antibody were used as the unlabeled control (black).
Background
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Function
K-Ras (KRAS) is a small GTPase that functions as a molecular switch within the RAS/MAPK signaling network, cycling between inactive GDP-bound and active GTP-bound states to regulate cell proliferation, differentiation, and survival[1][2]. Mechanistically, activated KRAS transduces signals from cell-surface receptors to downstream effectors, including the MAPK/ERK and PI3K/AKT pathways, thereby coordinating cellular growth and stress-response programs[1][3]. Oncogenic mutations impair GTP hydrolysis and maintain persistent KRAS signaling, resulting in sustained activation of proliferative pathways that contribute to tumor initiation, progression, and therapeutic resistance across multiple cancer types, particularly pancreatic ductal adenocarcinoma, colorectal cancer, and non-small cell lung cancer[2][3][4]. In disease models, mutant KRAS also reshapes the tumor microenvironment through inflammatory and immune-regulatory signaling, further supporting tumor development and immune evasion[3][2]. Compared with the related RAS isoforms HRAS and NRAS, KRAS is the most frequently altered RAS family member in human cancer and accounts for the majority of oncogenic RAS mutations, highlighting its distinct biological and clinical importance[2][5]. For experimental applications, the development of mutation-selective inhibitors, especially KRAS^G12C^ inhibitors, has established a tractable platform for studying KRAS-dependent signaling and therapeutic resistance mechanisms, although resistance remains a major challenge for long-term clinical efficacy[2][5].
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Subcellular Localization
Cell membrane,Endomembrane system,Cytoplasm, cytosol,Cell membrane
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Isoforms & Post-Translational Modification
P01116 has two isomers: P01116-1: 21656 Da (predicted); P01116-2: 21425 Da (predicted).
Acetylation at Lys-104 prevents interaction with guanine nucleotide exchange factors (GEFs)丨Palmitoylated at Lys-182, Lys-184 and Lys-185 (PubMed:29239724)丨Ubiquitinated by the BCR(LZTR1) E3 ubiquitin ligase complex at Lys-170 in a non-degradative manner, leading to inhibit Ras signaling by decreasing Ras association with membranes丨(Microbial infection) Glucosylated at Thr-35 by P -
Subunit
Interacts with PHLPP (By similarity)
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SwissProt ID
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Synonyms
c Ki ras2 antibody; c Kirsten ras protein antibody; c-K-ras antibody; c-Ki-ras antibody; Cellular c Ki ras2 proto oncogene antibody; Cellular transforming proto oncogene antibody; CFC2 antibody; cK Ras antibody; GTPase KRas antibody; K RAS p21 protein antibody; c Ki ras2 antibody; c Kirsten ras protein antibody
Documentation
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Data Sheet (259 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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User Guide for Antibodies (1077 KB)
[2]. Huang L, et al. KRAS mutation: from undruggable to druggable in cancer. Signal Transduct Target Ther. 2021 Nov 15;6(1):386. [Content Brief]
[3]. Uniyal P, et al. KRAS Mutations in Cancer: Understanding Signaling Pathways to Immune Regulation and the Potential of Immunotherapy. Cancers (Basel). 2025 Feb 25;17(5):785. [Content Brief]
[4]. Suda K, et al. Biological and clinical significance of KRAS mutations in lung cancer: an oncogenic driver that contrasts with EGFR mutation. Cancer Metastasis Rev. 2010 Mar;29(1):49-60. [Content Brief]
[5]. Riedl JM, et al. Emerging landscape of KRAS inhibitors in cancer treatment. Cancer Cell. 2026 Mar 9;44(3):471-497. [Content Brief]