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HRAS Antibody (YA6037)

(Synonyms: HRAS,HRAS1,GTPase,H-Ras-1,Ha-Ras,Transforming protein p21, ,c-H-ras, p21ras, Cleaved into: GTPase HRas N-terminally processed,Cleaved into: GTPase Hras,GTPase Hras,HRAS 1,)
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HRAS Antibody (YA6037) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to HRAS.

For research use only. We do not sell to patients.
  • Host:

    Rabbit

  • Isotype:

    IgG

  • Application:

    WB, IHC-P, ICC/IF, IP, ELISA

  • Reactivity :

    Human, Mouse, Rat

  • Formulation:

    Supplied in PBS, 50% glycerol, 0.05% Proclin 300, 0.05%BSA

  • Conjugation:
    Non-conjugated
  • HRAS Antibody (YA6037) Product Image
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To place orders, for customer services and technical support, please contact: MedChemExpress USA

Tel: 609-228-6898 E-mail: [email protected] [email protected]

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Use of MCE Products

Applications

Application
IHC-P Info
IHC-P: Immunohistochemistry-Paraffin
WB Info
WB: Western Blot
ICC/IF Info
ICC/IF: Immunocytochemistry/
Immunofluorescence
ELISA Info
ELISA: Enzyme Linked Immunosorbent Assay
IP Info
IP: Immunoprecipitation
Dilution Ratio 1:200-1:1000 1:2000-1:10000 1:200-1:1000 1:5000-1:20000 1:50-1:200

Product Details

Description

HRAS Antibody (YA6037) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to HRAS.

  • Host Rabbit
  • Clonality Monoclonal
  • Species Reactivity
    Human, Mouse, Rat
  • Observed Molecular Weight
    Observed band size: 21 kDa Info
    Note: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
  • Calculated Molecular Weight Predicted band size: 21 kDa
Purification

Protein A

Conjugation

Non-conjugated

Modification

Unmodified

Isotype

IgG

Product Properties

  • Appearance

    Solution

  • Formulation

    Supplied in PBS, 50% glycerol, 0.05% Proclin 300, 0.05%BSA

  • Concentration

    Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration

  • Storage & Stability

    Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.

  • Shipping

    Shipping with blue ice.

Background

  • Function

    H-Ras (HRAS) is a small GTPase that functions as a GDP/GTP-regulated molecular switch linking activated cell-surface receptors to intracellular signaling networks that control cell proliferation, differentiation, survival, and migration[4][5]. Mechanistically, H-Ras cycles between inactive GDP-bound and active GTP-bound states and transmits signals through major effector pathways, including the RAF-MEK-ERK and PI3K-AKT cascades, thereby coordinating growth factor-dependent cellular responses[6][1]. In disease contexts, activating HRAS mutations promote persistent downstream signaling and contribute to multiple human malignancies, with notable involvement in bladder, thyroid, head and neck, and oral squamous cell carcinomas[7][2]. Compared with related Ras isoforms, H-Ras, K-Ras, and N-Ras share highly conserved G-domains but differ substantially within their C-terminal hypervariable regions, which determine membrane trafficking, subcellular localization, and isoform-specific signaling outputs[4][8]. H-Ras is further distinguished by its dynamic palmitoylation-dependent trafficking between the plasma membrane and endomembrane compartments, enabling spatially restricted signal transduction and context-dependent biological effects[8][3]. These isoform-specific properties make H-Ras an important experimental model for dissecting Ras signaling compartmentalization and oncogenic network regulation[4][8]. For experimental and translational applications, H-Ras remains a particularly tractable therapeutic target because its membrane localization depends on farnesylation, and pharmacological farnesyltransferase inhibitors such as tipifarnib can suppress H-Ras-dependent signaling in selected tumor models[2][9].

  • Subcellular Localization

    Cell membrane; Lipid-anchor; Cytoplasmic side; Golgi apparatus; Golgi apparatus membrane; Lipid-anchor; Nucleus; Cytoplasm; Cytoplasm, perinuclear region

  • Expression


    Tissue_specificity:Broad expression

  • Isoforms & Post-Translational Modification

    P01112 has 2 isomers: P01112-1: 21298 Da (predicted); P01112-2: 18870 Da (predicted).
    Palmitoylated by the ZDHHC9-GOLGA7 complex. A continuous cycle of de- and re-palmitoylation regulates rapid exchange between plasma membrane and Golgi;S-nitrosylated; critical for redox regulation. Important for stimulating guanine nucleotide exchange. No structural perturbation on nitrosylation;The covalent modification of cysteine by 15-deoxy-Delta12,14-prostaglandin-J2 is autocatalytic and reversible. It may occur as an alternative to other cysteine modifications, such as S-nitrosylation and S-palmitoylation;Acetylation at Lys-104 prevents interaction with guanine nucleotide exchange factors (GEFs);Fatty-acylated at Lys-170;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;(Microbial infection) Glucosylated at Thr-35 by P.sordellii toxin TcsL (PubMed:19744486, PubMed:8626575, PubMed:8626586, PubMed:9632667). Monoglucosylation completely prevents the recognition of the downstream effector, blocking the GTPases in their inactive form, leading to inhibit Ras signaling (PubMed:8626575, PubMed:8626586, PubMed:9632667)

  • Subunit

    In its GTP-bound form interacts with PLCE1 (PubMed:11022048). Interacts with TBC1D10C (PubMed:17230191). Interacts with RGL3 (By similarity). Interacts with HSPD1 (By similarity). Found in a complex with at least BRAF, HRAS, MAP2K1, MAPK3 and RGS14 (By similarity). Interacts (active GTP-bound form) with RGS14 (via RBD 1 domain) (By similarity). Forms a signaling complex with RASGRP1 and DGKZ (PubMed:11257115). Interacts with RASSF5 (PubMed:18596699). Interacts with PDE6D (PubMed:11980706). Interacts with IKZF3 (PubMed:10369681). Interacts with RACK1 (PubMed:14500341). Interacts with PIK3CG; the interaction is required for membrane recruitment and beta-gamma G protein dimer-dependent activation of the PI3K gamma complex PIK3CG:PIK3R6 (By similarity). Interacts with RAPGEF2 (PubMed:10608844, PubMed:11598133). Interacts (active GTP-bound form) with both SHOC2 and PP1c (all isoforms) to form a tertiary complex; SHOC2 and PP1c preferably bind M-Ras/MRAS, but they also bind K-Ras/KRAS, N-Ras/NRAS and H-Ras/HRAS (PubMed:35768504, PubMed:35831509, PubMed:36175670). Interacts (GTP-bound form) with MAPKAP1/SIN1; inhibiting H-Ras/HRAS activity (PubMed:35522713)

  • SwissProt ID

    P01112

  • Gene ID
    3265 [NCBI]
  • Synonyms

    HRAS,HRAS1,GTPase,H-Ras-1,Ha-Ras,Transforming protein p21, ,c-H-ras, p21ras, Cleaved into: GTPase HRas N-terminally processed,Cleaved into: GTPase Hras,GTPase Hras,HRAS 1,

[1]. Hahn S M, et al. Farnesyltransferase inhibitors[C]//Seminars in oncology. WB Saunders, 2001, 28: 86-93.

[2]. Nussinov R, et al. Ras isoform-specific expression, chromatin accessibility, and signaling. Biophys Rev. 2021;13:489-505.

[3]. Adjei AA. Blocking oncogenic Ras signaling for cancer therapy. J Natl Cancer Inst. 2001 Jul 18;93(14):1062-74. doi: 10.1093/jnci/93.14.1062. PMID: 11459867. et al. Blocking oncogenic Ras signaling for cancer therapy. J Natl Cancer Inst. 2001 Jul 18;93(14):1062-74. [Content Brief]

[4]. Castellano E, et al. Functional specificity of ras isoforms: so similar but so different. Genes Cancer. 2011;2(3):216-231. [Content Brief]

[5]. Hobbs GA, et al. RAS isoforms and mutations in cancer at a glance. J Cell Sci. 2016;129(7):1287-1292. [Content Brief]

[6]. Czyzyk D, et al. Structural insights into isoform-specific RAS-PI3Kα interactions and the role of RAS in PI3Kα activation. Nat Commun. 2025 Jan 9;16(1):525. [Content Brief]

[7]. Mitin N, et al. Signaling interplay in Ras superfamily function. Curr Biol. 2005;15(14):R563-R574.

[8]. Johnson CW, et al. The small GTPases K-Ras, N-Ras, and H-Ras have distinct biochemical properties determined by allosteric effects. J Biol Chem. 2017;292(31):12981-12993.

[9]. Hoxhallari L, et al. Regulation of nucleotide excision repair by wild-type HRAS signaling in head and neck cancer. Cancer Gene Ther. 2025;32(6):662-677.

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HRAS Antibody (YA6037) Related Classifications

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100 mg

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Measured by its ability to inhibit anti-CD3-induced proliferation of stimulated CTLL-2 mouse cytotoxic T cells. The ED50 this effect is 0.8023 μg/ml, corresponding to a specific activity is 1246.42 units/mg.

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