HRAS Recombinant Monoclonal Antibody

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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HGNC: 5173

OMIM: 109800

KEGG: hsa:3265

STRING: 9606.ENSP00000309845

UniGene: Hs.37003