Recombinant Human Hepatocyte growth factor receptor(MET),partial (Active)

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Code CSB-AP003691HU
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  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
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Product Details

Purity Greater than 95% as determined by SDS-PAGE.
Endotoxin Less than 1.0 EU/μg as determined by LAL method.
Activity The ED50 as determined by its ability to bind Human HGF in functional ELISA is less than 10 ug/ml.
Target Names MET
Uniprot No. P08581
Research Area Signal Transduction
Alternative Names AUTS9; c met; D249; Hepatocyte growth factor receptor; HGF; HGF receptor; HGF/SF receptor; HGFR; MET; Met proto oncogene; Met proto oncogene tyrosine kinase; MET proto oncogene; receptor tyrosine kinase; Met proto-oncogene (hepatocyte growth factor receptor); Met proto-oncogene; Met protooncogene; MET_HUMAN; Oncogene MET; Par4; Proto-oncogene c-Met; RCCP2; Scatter factor receptor; SF receptor; Tyrosine-protein kinase Met
Species Homo sapiens (Human)
Source Mammalian cell
Expression Region 25-932aa
Mol. Weight 128.4 kDa
Protein Length Extracellular Domain
Tag Info C-terminal FC-tagged
Form Lyophilized powder
Buffer Lyophilized from a 0.2 μm filtered 1xPBS, pH 7.4
Reconstitution We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.
and FAQs
Protein FAQs
Storage Condition Store at -20°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time Basically, we can dispatch the products out in 5-10 working days after receiving your orders. Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Notes Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA Please contact us to get it.

Target Data

Function Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to hepatocyte growth factor/HGF ligand. Regulates many physiological processes including proliferation, scattering, morphogenesis and survival. Ligand binding at the cell surface induces autophosphorylation of MET on its intracellular domain that provides docking sites for downstream signaling molecules. Following activation by ligand, interacts with the PI3-kinase subunit PIK3R1, PLCG1, SRC, GRB2, STAT3 or the adapter GAB1. Recruitment of these downstream effectors by MET leads to the activation of several signaling cascades including the RAS-ERK, PI3 kinase-AKT, or PLCgamma-PKC. The RAS-ERK activation is associated with the morphogenetic effects while PI3K/AKT coordinates prosurvival effects. During embryonic development, MET signaling plays a role in gastrulation, development and migration of muscles and neuronal precursors, angiogenesis and kidney formation. In adults, participates in wound healing as well as organ regeneration and tissue remodeling. Promotes also differentiation and proliferation of hematopoietic cells. May regulate cortical bone osteogenesis (By similarity).
Gene References into Functions
  1. the miR-19a/c-Met pathway plays a critical role in acquired resistance to gefitinib and that the manipulation of miR-19a might provide a therapeutic strategy for overcoming acquired gefitinib resistance. PMID: 28592790
  2. The expression of C-Met and HER2 protein in lung adenocarcinoma is highly correlated, and whether it is synergistic in the targeted therapy of lung adenocarcinoma deserves further study. PMID: 29400000
  3. MET overexpression was more frequently found in high grade myxofibrosarcoma and the epithelioid variant. Chromosome 7 polysomy, rather than MET gene regional amplification, might account for the overexpression. of MET protein. PMID: 30126419
  4. miR-449a suppresses hepatocellular carcinoma tumorigenesis by down-regulating activity in the c-Met/ERK pathway. PMID: 30108016
  5. We found MET amplifications in two cases of endometrial clear-cell carcinoma with mixed features. PMID: 29633423
  6. Regarding gene mutation abundance, NGS enables the detection of low-abundant ctDNA in blood based on ultra-deep sequencing, and our patient benefited from crizotinib despite the low abundance of MET exon 14 skipping. These data indicate that we can choose targeted therapy despite the low abundance of gene mutations. PMID: 29110851
  7. The interplay of dual MET/HER2 overexpression in the AKT and ERK pathways for esophageal cancer is described. Therefore, combination therapy could be a novel strategy for EAC with amplification of both MET and HER2. PMID: 29223420
  8. MET inactivation in the context of the BRAF-activating mutation is driven through a negative feedback loop involving inactivation of PP2A phosphatase, which in turn leads to phosphorylation on MET inhibitory Ser985. PMID: 30224486
  9. MET Exon 14 Skipping Mutations in Non-small Cell Lung Cancer PMID: 30037377
  10. MET activation, by either METex14 mutations or amplification, is characteristic of a subset of early stage NSCLCs and may coexist with ERBB2 amplification. PMID: 29139039
  11. Results demonstrate that serum level of miR-658 is significantly lower in the NM group than in the DM group. Meanwhile, the levels of PAX3 and MET are lower in the NM group than in the DM group too. Both overexpression and silence of miR-658 significantly up-regulate or down-regulate the levels of PAX3 and MET in gastric cell lines. PMID: 29630524
  12. MiR-206 inhibits the development of epithelial ovarian cancer cell by directly targeting c-Met and inhibiting the c-Met/AKT/mTOR signaling pathway. PMID: 29807226
  13. These results suggest that gastric cancer progression is not associated with a unique signaling pathway and that a feedback loop may exist between the HGF/c-Met and Notch1 signaling pathways, which may result in therapeutic resistance. PMID: 29781036
  14. Comparative analysis revealed a strong association between MET expression and MET amplification (85% concurrence) in primary stomach tumors and matched liver metastasis. Survival analyses revealed that both MET amplification and MET overexpression were prognostic of poor outcomes. PMID: 29790169
  15. High c-met expression is associated with oral squamous cell carcinoma. PMID: 29286169
  16. FOXO1 serves as an important linker between HER2 and MET signaling pathways through negative crosstalks and is a key regulator of the acquired lapatinib resistance in HER2-positive GC cells. PMID: 28343375
  17. analysis of how the cMET blockade augments radiation therapy in patients with NF2 PMID: 29440379
  18. these findings highlight the relevance of cross-species protein interactions between murine feeder cells and human epithelial cells in 3T3-J2 co-culture and demonstrate that STAT6 phosphorylation occurs in response to MET activation in epithelial cells. However, STAT6 nuclear translocation does not occur in response to HGF, precluding the transcriptional activity of STAT6. PMID: 29771943
  19. c-Met-activated Mesenchymal Stem Cells (MSC) pre-exposed to hypoxia interact with PrPC at the site of ischemic injury to increase the efficiency of MSC transplantation. PMID: 29705776
  20. A novel G-quadruplex motif formed in the Human MET promoter region. PMID: 29054971
  21. a METex14 del mutation-positive NSCLC patient who responded to crizotinib but later relapsed, demonstrated a mixed response to glesatinib including reduction in size of a MET Y1230H mutation-positive liver metastasis and concurrent loss of detection of this mutation in plasma DNA. Together, these data demonstrate that glesatinib exhibits a distinct mechanism of target inhibition and can overcome resistance to PMID: 28765324
  22. This study demonstrates that simultaneous inhibition of c-Met and Src signaling in MD-MSCs triggers apoptosis and reveals vulnerable pathways that could be exploited to develop NF2 therapies. PMID: 28775147
  23. prolonged treatment of single HGF/c-Met or Hh inhibitor leads to resistance to these single inhibitors, likely because the single c-Met treatment leads to enhanced expression of Shh, and vice versa. Targeting both the HGF/c-Met and Hh pathways simultaneously overcame the resistance to the single-inhibitor treatment and led to a more potent antitumor effect in combination with the chemotherapy treatment. PMID: 28864680
  24. We identified unique and tumor-specific tyrosine phosphorylation rewiring in tumors resistant to treatment with the irreversible third-generation EGFR-inhibitor, osimertinib, or the novel dual-targeting EGFR/Met antibody, JNJ-61186372. PMID: 28830985
  25. TGF-beta negatively controls the HGF/c-MET pathway by regulating of stemness in glioblastoma. PMID: 29238047
  26. The preclinical efficacy and safety data provide a clear rationale for the ongoing clinical studies of Sym015 in patients with MET-amplified tumors. PMID: 28679766
  27. High MET expression is associated with malignant pleural mesothelioma. PMID: 28560410
  28. the results of real-time PCR and western blotting revealed that Huaier extract decreased p65 and c-Met expression and increased IkappaBalpha expression, while paclitaxel increased p65 expression and reduced IkappaBalpha and c-Met expression.The molecular mechanisms may be involved in the inhibition of the NF-kappaB pathway and c-Met expression PMID: 29039556
  29. Data found that the expression of c-Met was significantly increased in human oral squamous cell carcinoma (OSCC) tissues than in normal mucosa adjacent to the tumor, but was not correlated with clinicopathological parameters. Also, further findings indicated the potential role of c-Met in the progression of OSCC. PMID: 29115556
  30. Our data show that S49076 exerts its cytotoxic activity at low doses on MET-dependent cells through MET inhibition, whereas it inhibits growth of MET-independent cells at higher but clinically relevant doses by targeting Aurora B PMID: 28619752
  31. MET expression was shown to be significantly reduced in the superior temporal gyrus cortex of autism spectrum disorders individuals. PMID: 28322981
  32. In SCCHN, immunohistochemical overexpression of c-MET above cut-off levels III and particularly II was associated with inferior survival outcomes and advanced disease PMID: 29103754
  33. Here we present a case series of three such patients who achieved were cMET amplified and showed partial response on Crizotinib PMID: 29199685
  34. c-Met/beta1 integrin complex whose ligand-independent cross-activation and robust affinity for fibronectin drives invasive oncologic processes. PMID: 28973887
  35. tivantinib did not suppress MET signaling, and selective MET inhibitors demonstrated an antiproliferative effect only in MHCC97H, the unique cell line displaying MET gene amplification. HCC tumors with high expression of cell proliferation genes defined a group of patients with poor survival. PMID: 28246274
  36. Studies show that MET mutations have been found in cancer of unknown primary origin (CUP) being clustered to the SEMA and TK domain of the receptor. The biomechanical properties of MET mutants might trigger the hyper-invasive phenotype associated to CUP. [review] PMID: 29037604
  37. Data show that Kruppel like factor 4 (KLF4) was overexpressed in met proto-oncogene protein (c-Met)-overexpressing non-small-cell lung cancer (NSCLC) cells and tissues. PMID: 29624806
  38. SOCS1 attenuates migration and invasion properties of hepatocellular carcinoma cells at least partly via modulation of MET-mediated epithelial-mesenchymal transition, and controls invasive tumor growth. PMID: 29085209
  39. The authors reconfirmed EGFR mutation as a strong predictive marker of Non-Small-Cell Lung Cancer. However, c-MET positivity was not associated with response or progression-free survival, although c-MET overexpression correlated with some clinical characteristics. PMID: 29502124
  40. findings show oncogene E5 is primarily responsible for Met upregulation; E5-induced Met contributes motility of HPV-containing cells; these studies show a new role for E5 in epithelial-stromal interactions, with implications for cancer development PMID: 29609071
  41. EGFR T790M mutation and cMET amplification are main mechanisms leading to EGFR TKI resistance in lung adenocarcinoma. PMID: 29616327
  42. MET activation is associated with drug resistance in chronic myeloid leukemia. PMID: 28418880
  43. High glucose activated Met receptor in HK2 cells independently of HGF, via induction of integrin a5b1 and downstream signaling. This mode of Met activation was associated with tubular cell damage and apoptosis and it may represent a novel pathogenic mechanism and a treatment target in diabetic nephropathy. PMID: 28819999
  44. The purpose of this study was to explore gene copy number (GCN) variation of EGFR, HER2, c-MYC, and MET in patients with primary colorectal cancer. PMID: 28764718
  45. HGF/c-MET pathway mediates VEGFR inhibitor resistance and vascular remodeling in NSCLC. PMID: 28559461
  46. Because c-Met is strongly associated with pathological grade, stage and disease-specific survival, c-Met levels may have potential to predict patient prognosis and to guide clinical diagnosis and treatment of patients with renal cell carcinoma PMID: 28427859
  47. miR-1 is downregulated in ovarian cancer tissues, and may play a tumor suppressive role by inhibiting c-Met expression and its effects on the regulation of cell proliferation, migration and invasion PMID: 28698064
  48. Proto-oncogene proteins c-met (MET) mutations Y1248H and D1246N confer resistance in vitro and in vivo. PMID: 28396313
  49. MET overexpression is found in 23.8% of surgically resected NSCLC. MET amplification prevails in 4.6% and is associated with MET overexpression. Both have no influence on prognosis. PMID: 28838386
  50. study highlights the role of tissue differentiation on pathological response to neoadjuvant chemotherapy in gastric cancer and shows no impact between FOXP3, HER2 and MET expression in terms of tumor regression grading PMID: 29696715
  51. c-Met represents a prognostic marker in renal cell carcinoma.Furthermore, c-MET will play a decisive role as a possible target for targeted therapies in the era of personalised medicine. Especially for RCC, the dual inhibition of VEGF and c-MET tyrosine kinase in cases of metastatic, treatment-resistant tumours is gaining clinical relevance. The role of c-Met has not been fully elucidated for all subtypes of renal cell ca PMID: 28006830
  52. c-MET is a promising marker in K-RAS WT patients with colorectal liver metastases PMID: 28559118
  53. Results show that met protein is up-regulated with renal cell carcinoma and associated with poor prognosis. PMID: 28237182
  54. MET immunohistochemistry demonstrated 100% sensitivity and 70.4% specificity. Multivariate analyses showed that patients with METex14 skipping had a higher recurrence rate than those with ALK fusion (versus METex14 skipping) in stage I to IIIA disease; however, the differences in overall survival were not significant after adjustment for pathologic stage. PMID: 28502721
  55. In conclusion, these findings indicate that CMs derived from primary culture of NPC fractions of BA liver contain a large amount of active HGF, which may activate hepatic stem/progenitor cells and promote the appearance of hepatocyte-like cells or their clusters through HGF/c-Met signaling. PMID: 28364348
  56. despite the marginal occurrence of ALK gene amplification/high polisomy, we did not observed any ALK, MET and ROS deregulation in sarcomatoid carcinoma of head and neck PMID: 27262592
  57. Based on our study findings, SC patients should be screened for MET exon 14 mutations in the same manner as adenocarcinoma patients. PMID: 28418914
  58. These results hold promise that dual targeting of HGF and MET by combining extracellular ligand inhibitors with intracellular MET TKIs could be an effective intervention strategy for cancer patients who have acquired resistance that is dependent on total MET protein. PMID: 28341789
  59. The acquired sensitivity to erlotinib supports the known crosstalk between MET and the HER family of receptors. For the first time, we show inactivation of NF2 during acquisition of resistance to MET-TKI that may explain the refractoriness to erlotinib in these cells. PMID: 28396363
  60. c-MET phosphorylation is regulated by autophagy via an mTORC2-dependent mechanism. PMID: 28475179
  61. Fusion of TPR(2-142) protein to the MET intracellular domain strongly and selectively stabilizes the alphaG helix of the MET kinase domain. PMID: 28528776
  62. cabozantinib suppressed MMP1 expression by blocking HGF-MET signaling and that HGF-MET-MMP1 signaling is involved in the invasiveness and proliferation of BCa cells. These results suggest that cabozantinib might prove useful for future treatment of muscle-invasive BCa. PMID: 28013036
  63. Our data reveal that clear-cell RCC with MET upregulation show an aggressive behavior and MET copy number increase is evident in a substantial percentage of patients with high-grade carcinomas and metastatic disease. PMID: 27894094
  64. These findings indicate that RON and c-Met facilitate metastasis through ERK1/2 signaling and that targeting RON and c-Met with foretinib may be an attractive therapeutic option for suppressing Prostate cancer metastasis PMID: 28440432
  65. IGF1R signaling under the given experimental conditions and NSCLC genetic background dictates the functional endpoint mechanism for TKI resistance. Manipulating this regulatory role of IGF1R can force the functional endpoint mechanism for TKI resistance in a defined and targetable direction here illustrated by the observed MET-amplification. PMID: 28418902
  66. MET status in CTCs isolated on ISET filters from blood samples of advanced-stage NSCLC patients correlated strongly with MET status in tumor tissue, illustrating the potential for using CTCs as a non-invasive, real-time biopsy to determine MET status of patients entering clinical trials. PMID: 28212540
  67. Data show that c-MET gene amplification was detected more frequently in metastatic lymph nodes than in primary cancerous tissue which suggests that lymph node metastasis can predict c-MET gene amplification in a primary tumor. PMID: 28590585
  68. MET-positive gastric cancers (GCs) had a very poor prognosis, with a median survival of 5.4 months and a hazard ratio of 2.126. A combination of immunohistochemistry and chromogenic in-situ hybridization (CISH) is suitable to assess MET status. PMID: 26033401
  69. Collectively, we demonstrated that c-Met signalling induced lamellipodia formation by upregulating lamellipodin, thereby promoting the migration of oral squamous cell carcinoma cells. PMID: 28440510
  70. Ran GTPase promotes cancer progression via Met recepto-rmediated downstream signaling PMID: 27716616
  71. Transcriptional upregulation of MET is a key molecular event associated with colorectal cancer invasion and tumor budding. PMID: 27793046
  72. MET gene amplification was the main reason for MET overexpression in gastric adenocarcinoma. PMID: 28052014
  73. RAS mutations and HER2/MET amplification were the most frequently detected resistance mechanisms in both tissue and blood sample analysis. On the other hand, BRAF and EGFR ectodomain mutations were much rarer.The combined analysis of tissue and blood (ctDNA) results highlights the complexity of clonal evolution triggered by EGFR blockade PMID: 27780856
  74. Malignant melanoma has the ability to undergo phenotypic change by a cell-intrinsic/autonomous mechanism that can be characterized by Met expression. PMID: 27683122
  75. Findings suggest that MET rs1621 polymorphism, alone and combined with miR-199a rs74723057, may influence susceptibility to hepatocellular carcinoma. PMID: 27813498
  76. ABBV-399 represents a novel therapeutic strategy to deliver a potent cytotoxin to c-Met-overexpressing tumor cells enabling cell killing regardless of reliance on MET signaling. ABBV-399 has progressed to a phase I study where it has been well tolerated and has produced objective responses in c-Met-expressing non-small cell lung cancer (NSCLC) patients. PMID: 27573171
  77. High CD44 expression is associated with high c-MET expression, p16-negative tumors, and EGFR-positive tumors. The combination of these markers predicts for poor prognosis in HNSCC patients treated with chemoradiation. PMID: 27442811
  78. MET/T790M-positive patients are at higher risk of acquired resistance to EGFR-Tyrosine kinase inhibitors, and have a worse Post-progression survival than patients with only MET overexpression or the T790M mutation alone. Clinical trials are needed to determine the best treatment for patients with both MET overexpression and the EGFR T790M mutation. PMID: 27259997
  79. revealed that salvianolic acid A enhanced sensitivity to cisplatin in A549/DDP cells mainly through suppression of the c-met/AKT/mTOR signaling pathway PMID: 28939129
  80. For intra-hepatic cholangiocarcinomas (IHCC)patients, ROS1, ALK and c-MET expression levels have prognostic significance on clinical outcomes. Although this finding may require further validation, it has led to proposal of a new stratification or enriched biomarker for future phase III trial of anti-EGFR therapy in IHCC. PMID: 27136744
  81. The high incidence of METDelta14 mutation in sarcomatoid carcinoma suggested that MET inhibition might benefit this specific subgroup of patients. PMID: 26847053
  82. Data show that MET amplification identified by circulating-free DNA (cfDNA) occurred in a sizable subset of patients that are refractory to anti-EGFR therapy. PMID: 27421137
  83. Data suggest palmitoylation is required for egress from the Golgi for transport to the plasma membrane. These findings introduce palmitoylation as a critical modification of c-Met. PMID: 27081699
  84. our studies for the first time establish p100 as a key tumor suppressor of bladder cancer growth PMID: 27147579
  85. Her2, cMet and FGFR2 statuses were profiled in gastric cancer (GC) patients and the -derived tumor xenograft(PDX) models. PMID: 28292264
  86. Full-length MET was quantifiable in 5 of 5 core needle samples. PMID: 27001313
  87. Cells with ectopic FOXM1 expression demonstrate considerable ( approximately 20%, P < 0.001) growth advantage despite MET targeting. PMID: 27185371
  88. MET was almost exclusively expressed in HRPC and prostate cancer bone metastasis, but was not related to MET amplification or polysomy. PMID: 27105539
  89. study presents the unique characteristics of MET exon 14 mutations in Chinese patients with non-small-cell lung cancer (NSCLC); found no significant relationships among the mutation, MET amplification, and MET overexpression; MET exon 14 mutation per se may not be sufficiently robust for use in defining a subset of NSCLCs PMID: 27257131
  90. MET exon 14 skipping was detected in 1.3% (23/1770) of the Chinese patients with Non-Small Cell Lung Cancer (NSCLC). MET exon 14 skipping defined a new molecular subset of NSCLC with identifiable clinical characteristics. The therapeutic EGFR inhibitors might be an alternative treatment for patients with MET mutant NSCLC. PMID: 27223439
  91. FKBP12 binding is required for full Met activation and everolimus can inhibit Met PMID: 27223077
  92. c-Met may have a role in response to EGFR-TKI treatment in advanced non-small cell lung cancer PMID: 27213587
  93. Study shows that Met and HGF have a multi-factorial relationship to the biology and outcome of breast cancer, influenced by gene copy number and protein expression, activation status, stromal environment, and cellular localisation PMID: 27175600
  94. This highlights the importance of correctly selecting biomarkers for targeted therapies. A multivariate analysis suggested that MET positivity may still be prognostic for worse median overall survival in gastric cancer; therefore, it is important to continue investigation into the optimal approach to inhibit MET signaling in gastric cancer. PMID: 27401892
  95. The results of this study showed that expression of MET showed a significant increase (p = 0.011) at recurrence after radiotherapy-temozolomide. PMID: 27566180
  96. MET mutation was detected by qRT-PCR in all samples with heterogeneous MET expression microdissected from five cases with MET-mutated adenocarcinoma, while MET gene amplification was detected in tumor areas expressing high MET protein levels among MET-mutated adenocarcinomas. PMID: 28285687
  97. The oleocanthal-based homovanillyl sinapate is a novel c-Met inhibitor which reduced tumor growth orthotopic model of triple negative breast cancer. PMID: 27086914
  98. Studies indicate that miR-182 negatively regulated Met via direct binding to the Met 3'-untranslated region (3'-UTR). PMID: 28940757
  99. Selective MET tyrosine kinase inhibitor SAR125844 has significant antitumour activity in patients with MET-amplified non-small cell lung carcinoma. PMID: 29145039
  100. miR-34a reconstitution in DMPM cells significantly inhibited proliferation and tumorigenicity, induced an apoptotic response, and declined invasion ability, mainly through the down-regulation of c-MET and AXL and the interference with the activation of downstream signaling. PMID: 28100259

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Involvement in disease Hepatocellular carcinoma (HCC); Renal cell carcinoma papillary (RCCP); Deafness, autosomal recessive, 97 (DFNB97); Osteofibrous dysplasia (OSFD)
Subcellular Location Membrane, Single-pass type I membrane protein, SUBCELLULAR LOCATION: Isoform 3: Secreted
Protein Families Protein kinase superfamily, Tyr protein kinase family
Tissue Specificity Expressed in normal hepatocytes as well as in epithelial cells lining the stomach, the small and the large intestine. Found also in basal keratinocytes of esophagus and skin. High levels are found in liver, gastrointestinal tract, thyroid and kidney. Also
Database Links

HGNC: 7029

OMIM: 114550

KEGG: hsa:4233

STRING: 9606.ENSP00000317272

UniGene: Hs.132966

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