HRAS Antibody, Biotin conjugated

Code CSB-PA010726LD01HU
Size US$299
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Product Details

Full Product Name Rabbit anti-Homo sapiens (Human) HRAS Polyclonal antibody
Uniprot No. P01112
Target Names HRAS
Alternative Names C BAS/HAS antibody; C HA RAS1 antibody; C-BAS/HAS antibody; c-H-ras antibody; C-HA-RAS1 antibody; CTLO antibody; GTPase HRas antibody; GTPase KRas antibody; GTPase NRas antibody; H ras antibody; H RASIDX antibody; H-Ras-1 antibody; H-RASIDX antibody; Ha-Ras antibody; HAMSV antibody; HRAS antibody; HRAS1 antibody; K ras antibody; K RAS2A antibody; K RAS2B antibody; K RAS4A antibody; K RAS4B antibody; K-RAS antibody; KRAS antibody; KRAS1 antibody; KRAS2 antibody; N-RAS antibody; N-terminally processed antibody; NRAS antibody; NRAS1 antibody; p21ras antibody; RASH_HUMAN antibody; RASH1 antibody; RASK2 antibody; Transforming protein p21 antibody; v Ha ras Harvey rat sarcoma viral oncogene homolog antibody; v Ki ras2 Kirsten rat sarcoma viral oncogene homolog antibody; v ras neuroblastoma RAS viral oncogene homolog antibody
Raised in Rabbit
Species Reactivity Human
Immunogen Recombinant Human GTPase HRas protein (12-181AA)
Immunogen Species Homo sapiens (Human)
Conjugate Biotin
Clonality Polyclonal
Isotype IgG
Purification Method >95%, Protein G purified
Concentration It differs from different batches. Please contact us to confirm it.
Buffer Preservative: 0.03% Proclin 300
Constituents: 50% Glycerol, 0.01M PBS, PH 7.4
Form Liquid
Tested Applications ELISA
Protocols ELISA Protocol
Troubleshooting and FAQs Antibody FAQs
Storage Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
Lead Time Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.

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Target Background

(From Uniprot)
Involved in the activation of Ras protein signal transduction. Ras proteins bind GDP/GTP and possess intrinsic GTPase activity.
Gene References into Functions
  1. results demonstrate that adenomyoepitheliomas are genetically heterogeneous, and qualify mutations in HRAS, a gene whose mutations are vanishingly rare in common-type breast cancers, as likely drivers of ER-negative adenomyoepitheliomas PMID: 29739933
  2. Plasma membrane polyphosphoinositides depletion caused rapid translocation of K-Ras4B but not H-Ras from the plasma membrane to the Golgi. PMID: 28939768
  3. Data show that an indispensable beta-subunit of the voltage-gated Ca(2+) channel Cav1.2 interaction with H-Ras is independently of Ca(2+) flux, suggesting the regulatory role of beta2 in transcriptional activation via the ERK/CREB pathway. PMID: 30150369
  4. This study demonstrated that Oligodendrocyte RasG12V expressed in its endogenous locus disrupts myelin structure through increased MAPK, nitric oxide, and notch signaling. PMID: 28856719
  5. Data indicate dynamic of H-Ras functional cycle as controlled by son of sevenless homolog 1 (Sos). PMID: 27412770
  6. Our data support the idea that a variable range of dysregulated HRAS-dependent signalling dynamics, rather than static activation of HRAS-dependent signal flow, may underlie the phenotypic variability in CS. PMID: 28139825
  7. AF6 employs a non-canonical, evolutionarily conserved alpha-helix to bind RAS, unique to AF6 and the classical RASSF effectors. PMID: 29062045
  8. Case Report: somatic HRAS mutation in pigmented trichoblastoma developed in a sebaceous nevus. PMID: 28554764
  9. our identification of the novel interaction between Aurora A and H-Ras as a mechanism by which Aurora A can activate Ras-MAPK signaling opens the way for studies into perturbation of the Aurora A/H-Ras interaction and the effect on Ras-MAPK signaling. PMID: 28177880
  10. Peroxiredoxin I (Prx I) increased in tumors of hepatocellular carcinoma (HCC) patients that aligned with overexpression of oncogenic H-ras. PMID: 27517622
  11. Familial alcohol dependence was associated with hypomethylation of CpG sites in the HRAS promoter region. PMID: 28799801
  12. Suppression of MEK/ERK pathway in senescent cells provides a new strategy for elimination of Ras-expressing cells. PMID: 29140794
  13. ESR1 inhibits senescence-like phenotype and facilitates transformation induced by oncogenic ras in human mammary epithelial cells PMID: 27259243
  14. Data show that STK38 supports Ras-driven transformation through promoting detachment-induced autophagy. PMID: 27283898
  15. Data indicate acquired KRAS, NRAS or HRAS mutations in more than one third of patients after cetuximab exposure. PMID: 27119512
  16. HRAS mutations were more common in epithelial-myoepithelial carcinomas (EMCAs) with intact PLAG1 and HMGA2. Most EMCAs arose ex pleomorphic adenoma (PA)and the genetic profile of EMCA varies with the absence or presence of preexisting PA and its cytogenetic signature. Progression to higher grade EMCA with intact PLAG1 and HMGA2 correlates with the presence of TP53, FBXW7 mutations, or SMARCB1 deletion. PMID: 29135520
  17. Analysis of HRAS mutations and their respiratory phenotype revealed that the common p.Gly12Ser mutation is more often associated with transient respiratory distress and other respiratory diagnoses. PMID: 27102959
  18. we found that H-Ras proteins and particularly the G12V and G13D variants are significantly more flexible than their K-Ras counterparts.while most of the simulated proteins sampled the effector-interacting state 2 conformational state, G12V and G13D H-Ras adopted an open switch state 1 conformation that is defective in effector interaction PMID: 28498561
  19. The HRAS mutation p.T58I could manifest with severe early-onset but stabilizing cardiomyopathy. The dysmorphic features are mild compared with the features of Costello syndrome. The phenotypic variability makes the diagnosis challenging, suggesting that this variant of Costello syndrome might go undiagnosed. PMID: 26888048
  20. Age at diagnosis of follicular thyroid cancer (FTC) and frequency of extrathyroidal extension have changed over four decades; prevalence of RAS mutations has decreased; HRAS/NRAS (codon 61) and TERT (promoter) mutations may be associated with poor clinical outcomes in FTC, especially when two mutations coexist; this retrospective study was conducted in Seoul. PMID: 28864536
  21. Knockdown of forkhead Box M1 (FoxM1) reduced Prx II levels in H-ras(G12V)-hepatocellular carcinoma (HCC) cells, indicating FoxM1 as a direct transcription factor of Prx II in HCC. PMID: 26500057
  22. we found that ectopic expression of oncogenic KRas and HRas in cells resulted in elevated CIB1 expression. We previously described the Ca(2+)-myristoyl switch function of CIB1, and its ability to facilitate agonist-induced plasma membrane localisation of sphingosine kinase 1 (SK1), a location where SK1 is known to elicit oncogenic signalling. PMID: 27941888
  23. Data suggest that isoform-specific sequences in the allosteric lobes of HRAS, KRAS, and NRAS have an impact on biocatalysis (kinetics of GTP hydrolysis) and interaction with c-Raf kinase, which must be due to allosteric effects on dynamics and conformational states, given the identical active sites of these isoenzymes. PMID: 28630043
  24. Data suggest HRas activates both p110alpha and p110delta isoforms; membrane-resident HRas, not soluble HRas, increases membrane recruitment of both p110alpha and p110delta. (HRas = v-Ha-ras Harvey rat sarcoma viral oncogene homolog; p110alpha = class IA phosphoinositide 3-kinases, subunit p110alpha; p110delta = class IA phosphoinositide 3-kinases, subunit p110delta) PMID: 28515318
  25. Our data suggest that testing for any RAS mutation is unlikely to change the clinical management of thyroid nodules that have indeterminate cytology PMID: 28116986
  26. Equilibrium dissociation constants were determined for the binding of HRAS, KRAS, NRAS and RRAS2 to the RAS binding (RB) domain of binding proteins. PMID: 27936046
  27. Studies indicate that RAS proteins were among the first oncogenes identified and are mutationally activated in 30% of all cancer types. PMID: 28202657
  28. 6 of 7 (86%) malignant ectomesenchymomas had HRAS mutations PMID: 26872011
  29. RAS-positive thyroid cancer most often demonstrates indolent sonographic features and more commonly associates with lower risk, "indeterminate" cytology. PMID: 27689252
  30. Studies indicate that the control of spatiotemporal RAS protein signalling show that activation kinetics and subcellular compartmentalisation are tightly coupled to the generation of specific biological outcomes. PMID: 27911734
  31. HRAS mutation is associated in children with delayed puberty and probably with precocious puberty. PMID: 27940666
  32. HRAS mutation is associated with salivary duct carcinoma. PMID: 27379604
  33. Impact of SNPs on CpG Islands in the MYC and HRAS oncogenes and in a wide variety of tumor suppressor genes has been analyzed in a multi-cancer bioinformatics approach. PMID: 27074591
  34. Ras isoforms' dimer conformations are not uniform; instead, the isoform-specific dimers reflect the favoured interactions of the HVRs (hypervariable regions) with cell membrane microdomains, biasing the effector-binding site orientations, thus isoform binding selectivity. PMID: 27057007
  35. Two unrelated boys with Costello syndrome and an HRAS mutation (p.Gly13Cys) are presented with their ophthalmologic findings. Both had early symptoms of nystagmus, photophobia, and vision abnormalities PMID: 28337834
  36. The fact that no malignant tumors were described in these individuals does not allow definitive conclusions about the risk for cancer development. It remains to be determined if substitutions of amino acid 13 in HRAS (p.Gly13Asp and p.Gly13Cys) increase the risk of tumor development PMID: 28371260
  37. Overexpression of K-p21Ras was found in all colorectal cancer tissues tested, overexpression of N-p21Ras was found in 85.7% of the colorectal cancertissues, while H-p21Ras expression was not found in any colorectal cancer tissue. PMID: 28259994
  38. herefore, our results also demonstrate that the phenotype in CS and somatic cancers is not only determined by the different transforming potentials of mutant HRAS proteins, but also by the efficiency of exon 2 inclusion resulting from the different HRAS mutations. PMID: 27195699
  39. Point mutations of HRAS is associated with thyroid cancer. PMID: 27535135
  40. The results show that mutant RAS is associated with an earlier and higher rate of local tumour progression in patients undergoing ablation of CLMs. PMID: 28240361
  41. A report of three cases with pediatric urothelial bladder cancer indicates that the tumors are characterized by a consistent H-RAS mutation status, whereas FGFR3 and p53 pathways are not involved in this tumor initiation. PMID: 26522772
  42. The coexistence of BRAF or RAS mutations enhanced the prognostic effects of telomerase reverse transcriptase (TERT) promoter mutations. Furthermore, TERT promoter mutations strengthened the predictions of mortality and recurrence by the ATA and TNM staging systems, particularly for high-risk patients with differentiated thyroid cancer. PMID: 26969876
  43. Overexpression of HRAS is associated with Breast Cancer Recurrence. PMID: 27165221
  44. Study acts as a further supplement of the genetic features of neuroendocrine tumors. Somatic mutations of three potential tumor-related genes (HRAS, PAK1 and MEN1) might contribute to the tumorigenesis of thymic neuroendocrine tumors with EAS. PMID: 27913610
  45. Activating HRAS, KRAS and EGFR mutations play a major role in the pathogenesis of sporadic SGH. These results support the concept that SGH is a true benign neoplasm rather than a reactive hyperplasia. PMID: 26804118
  46. HRAS mutation is associated with liver cancer. PMID: 26799184
  47. findings support a role of HRAS mutations as a somatic driver event in benign PPGL without other known susceptibility gene mutations. HRAS mutated PPGL cluster together with NF1- and RET-mutated tumors associated with activation of kinase-signaling pathways PMID: 26773571
  48. Ras activity fine tunes the period length and modulates photoentrainment of the circadian clock. PMID: 25762011
  49. mTOR kinase inhibitor pp242 causes mitophagy terminated by apoptotic cell death in E1A-Ras transformed cells. PMID: 26636543
  50. Data show that Ba/F3 cells transformed with mutant HRAS protien indicated equal sensitivity towards Map kinase kinase (MEK) and mTOR serine-threonine kinase (mTOR) inhibition. PMID: 26544513

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Involvement in disease Costello syndrome (CSTLO); Congenital myopathy with excess of muscle spindles (CMEMS); Thyroid cancer, non-medullary, 2 (NMTC2); Bladder cancer (BLC); Schimmelpenning-Feuerstein-Mims syndrome (SFM)
Subcellular Location Cell membrane; Lipid-anchor; Cytoplasmic side. Golgi apparatus. Golgi apparatus membrane; Lipid-anchor.; [Isoform 2]: Nucleus. Cytoplasm. Cytoplasm, perinuclear region. Note=Colocalizes with RACK1 to the perinuclear region.
Protein Families Small GTPase superfamily, Ras family
Tissue Specificity Widely expressed.
Database Links

HGNC: 5173

OMIM: 109800

KEGG: hsa:3265

STRING: 9606.ENSP00000309845

UniGene: Hs.37003


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