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Validated All-in-One™ qPCR Primer for PTH1R(NM_001184744.1) Search again
Product ID:
HQP064213
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
EKNS, PFE, PTHR, PTHR1
Gene Description:
parathyroid hormone 1 receptor
Target Gene Accession:
NM_001184744.1(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
The protein encoded by this gene is a member of the G-protein coupled receptor family 2. This protein is a receptor for parathyroid hormone (PTH) and for parathyroid hormone-like hormone (PTHLH). The activity of this receptor is mediated by G proteins which activate adenylyl cyclase and also a phosphatidylinositol-calcium second messenger system. Defects in this receptor are known to be the cause of Jansen's metaphyseal chondrodysplasia (JMC), chondrodysplasia Blomstrand type (BOCD), as well as enchodromatosis. [provided by RefSeq].
Gene References into function
- different domains of PTHR implicated in agonist-dependent receptor internalization; the receptor's core (Asn-289 and Lys-382) appears to regulate internalization of the receptor/beta-arrestin complex toward early endocytic endosomes during endocytosis.
- mutant expression in enchondromatosis
- Na(+)/H(+ ) exchanger regulatory factor 2 directs parathyroid hormone 1 receptor signalling
- These results show how specific interactions between PTH1Rc and its ligands may stabilize distinct conformational states, representing either the active G protein-coupled or a desensitized beta-arrestin-coupled receptor state.
- vascular sites of expression of PTHrP and its cognate receptor in the rheumatoid synovium and/or in cultured rheumatoid synovial endothelial cells
- expression is preserved in the growth plate of human fetuses affected with fibroblast growth factor receptor type 3 activating mutations
- The juxtamembrane region of the PTH-1 receptor interacts with parathyroid hormone (PTH) via a mechanism that involves the N-terminal portion of the ligand and residues 15-20, particularly residue 19, of PTH.
- The parathyroid hormone-related protein receptor is expressed in breast cancer bone metastases and promotes autocrine proliferation in breast carcinoma cells.
- collagenases can be a downstream effector of PTH/PTHrP receptor action in trabecular bone, but not in periosteum.
- Binds to a specific sites of PTH-related protein.
- PTHrP is an essential growth factor for clear cell renal carcinoma and is a novel target for the von Hippel-Lindau tumor suppressor protein.
- factors present in uremia hemodialysis ultrafiltrate decrease PTH-stimulated cAMP generation by a mechanism that involves a decrease in the levels of PTH1R mRNA levels.
- The PTH1R C terminus contains regulatory sequences that are involved in, but not required for, PTH1R internalization. The results demonstrate that receptor activation and internalization can be selectively dissociated.
- haplotype frequencies and linkage disequilibrium (LD) analysis of four different polymorphisms at the PTHR1 locus
- results indicate that the PTHR1 gene is not the culprit for enchondromatosis
- GSK3 and PKB/Akt have roles in the integrin-mediated regulation of PTHrP, IL-6 and IL-8 in pancreatic cancer
- PTH1R trafficking and G(q) (but not G(s)) signaling independently contribute to ERK1/2 activation, predominantly via transactivation of the epidermal growth factor receptor.
- PTH1R cytoplasmic tail interacts with calmodulin in a calcium-dependent manner via the basic 1-5-8-14 motif
- Cytoskeletal protein 4.1G facilitates the cell-surface localization of PTHR through its interaction with the C-terminus of the receptor, resulting in the potentiation of PTHR-mediated signal transduction.
- Cytoskeletal protein 4.1G facilitates the cell-surface localization of PTHR through its interaction with the C-terminus of the receptor, resulting in the potentiation of PTHR-mediated signal transduction.[cytoskeletal protein 4.1G]
- Manumycin inhibits cell proliferation and decreases PTHrP levels in anaplastic thyroid cancer cells in vitro and in vivo and decreases the PTHrP level in the nucleus.
- the conformational change that switches the receptor into its active state proceeds in a sequential manner, with the first rapid binding step event preceding receptor activation by PTH(1-34)
- Review. The multiple roles of PTHR1 in cell differentiation & proliferation in many organs, especially endochondral bone, and chondrodysplasias due to its mutation are reviewed.
- beta-arrestin and G proteins activate parathyroid hormone receptor-stimulated ERK1/2 pathways
- CCN2 was critically involved in osteolytic metastasis and was induced by PKA- and PKC-dependent activation of ERK1/2 signaling by PTHrP.
- PTHrP, TGF-beta1, and VEGF expression was significantly altered and indicated degenerative changes in Kashin-Beck disease cartilage
- data delineate multiple PTH1R structural determinants for ERK1/2 activation and identify unique mechanism involving proline-rich motifs in receptor C terminus for reciprocal scaffolding of c-Src and beta-arrestin2 with class II G-protein-coupled receptor
- PTHrP induces HHM and concurrent cachectic syndromes by mechanisms other than directly modulating the leptin or hypothalamic feeding-regulated peptides
- cysteine at position 217 in plays a critical role in translocation to the cell surface and biological function of PTHR1
- Increased cell survival, migration, invasion, and Akt expression were studied in PTHR-overexpressing LoVo colon cancer cell lines.
- Coexpression of Etsl and CBP induced a synergistic activation of the parathyroid hormone-related protein P3 promoter only in the tumorigenic cell line.
- Modulation of cell adhesion is a normal physiological action of parathyroid hormone, mediated by increasing integrin gene transcription.
- PTHR1 over-expression may promote osteosarcoma progression by conferring a more aggressive phenotype, and forming a more favorable microenvironment
- constitutive activation of PTH/PTHrP receptor signaling in osteoblastic cells suppresses unloading-induced bone loss specifically through the regulation of osteoclastic activity.
- A microtubule-facilitated nuclear import pathway for PTHR is descibed.
- Results conclude that PTH and PTHrP bind similarly to the G protein-coupled PTHR conformation, PTH has a greater capacity to bind to the G protein-uncoupled conformation.
- that NHERF1 inhibits endocytosis without affecting PTH1R recycling
- PTHR1 polymorphisms influence bone density variation through effects on the growing skeleton.
- findings suggest that one of the pathways via which 1,25(OH)(2)D(3) exerts its anti-proliferative effects is through down-regulation of PTHrP expression
- These data indicate that PTHrP contributes to the malignancy of oral cancers downstream of EGFR signaling, and may thus provide a therapeutic target for oral cancer.
- 6 SNPs in the PTH gene and 3 SNPs each in the PTHLH, PTHR1 and PTHR2 genes were investigated in relation to bone mineral density
- 1.95-A structure of PTH bound to the MBP-PTH1R-extracellular domain fusion
- PTH/PTHrP receptor in MCF7 cells has higher binding affinity for PTHrP than PTH compared to the receptor in SaOS-2 cells
- Different receptor subtype properties were used to demonstrate that residue 41 in PTH-1R, when either the native Leu or substituted by Ile or Met, can accommodate either Phe or Trp at position 23 of the ligand.
- These data demonstrate that PTHrP and its receptor are up-regulated specifically during immortalization of T-lymphocytes by HTLV-1 infection and may facilitate the transformation process.
- PTHR1 functionally deleterious mutations have now been identified in five out 31 enchondromas from Ollier patients.
- In transgenic mice, signaling in osteocytes increases bone mass and the rate of bone remodeling.
- the putative R(0) PTHR conformation can form highly stable complexes with certain PTH ligand analogs and thereby mediate surprisingly prolonged signaling responses in bone and/or kidney PTH target cells
- PTHR1 loss-of-function mutations in familial, nonsyndromic primary failure of tooth eruption are reported.