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Rabbit Polyclonal Phospho-Flg (Y154) antibody (STJ90678)
Supplier: St John’s Laboratory Ltd.
Recommended applications: WB, IF, ELISA
Recommended dilution: WB 1:500-1:2000; IF 1:200-1:1000; ELISA 1:40000;
Recommended protocols: check protocols
Click or hover above images to see image description for Flg (phospho Tyr154) Polyclonal Antibody.
Check alternative names for the antibodyExpand
FGFR1 antibody, BFGFR antibody, CEK antibody, FGFBR antibody, FLG antibody, FLT2 antibody, HBGFR antibody,|Basic fibroblast growth factor receptor 1 antibody|HBGFR antibody|heparin-binding growth factor receptor antibody|HH2 antibody|HRTFDS antibody|hydroxyaryl-protein kinase antibody|KAL2 antibody|N-SAM antibody|OGD antibody|Proto-oncogene c-Fgr antibody|Anti-FGFR1 antibody – ChIP Grade (ab10646)
SCBT cat No: sc-121|sc-393911|sc-7945|sc-57132|sc-57133|sc-31169|sc-134223|sc-53826|sc-356|
Flg (phospho Tyr154) Polyclonal Antibody
|Catalogue No.|| |
Human, Mouse, Rat
Phospho-Flg (Y154) Polyclonal Antibody detects endogenous levels of Flg protein only when phosphorylated at Y154.
Synthesized phospho-peptide derived from Flg (phospho Tyr154) at AA range 90-170
WB, IF, ELISA
|Recommended dilution|| |
WB 1:500-1:2000; IF 1:200-1:1000; ELISA 1:40000;
|Molecular weight|| |
Flg (phospho Tyr154) Antibody was tube-contained. Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Flg (phospho Tyr154) Antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Alternative antibody names|| |
Fibroblast growth factor receptor 1 antibody, FGFR-1 antibody, Basic fibroblast growth factor receptor 1 antibody, BFGFR antibody, bFGF-R-1 antibody, Fms-like tyrosine kinase 2 antibody, FLT-2 antibody, N-sam antibody, Proto-oncogene c-Fgr antibody, CD antigen CD331 antibody
|Protein names|| |
Fibroblast growth factor receptor 1 , FGFR-1 , Basic fibroblast growth factor receptor 1 , BFGFR , bFGF-R-1 , Fms-like tyrosine kinase 2 , FLT-2 , N-sam , Proto-oncogene c-Fgr , CD antigen CD331
|Protein function|| |
Tyrosine-protein kinase that acts as cell-surface receptor for fibroblast growth factors and plays an essential role in the regulation of embryonic development, cell proliferation, differentiation and migration. Required for normal mesoderm patterning and correct axial organization during embryonic development, normal skeletogenesis and normal development of the gonadotropin-releasing hormone (GnRH) neuronal system. Phosphorylates PLCG1, FRS2, GAB1 and SHB. Ligand binding leads to the activation of several signaling cascades. Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate. Phosphorylation of FRS2 triggers recruitment of GRB2, GAB1, PIK3R1 and SOS1, and mediates activation of RAS, MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway. Promotes phosphorylation of SHC1, STAT1 and PTPN11/SHP2. In the nucleus, enhances RPS6KA1 and CREB1 activity and contributes to the regulation of transcription. FGFR1 signaling is down-regulated by IL17RD/SEF, and by FGFR1 ubiquitination, internalization and degradation. / ATP + a [protein]-L-tyrosine = ADP + a [protein]-L-tyrosine phosphate. / Present in an inactive conformation in the absence of bound ligand. Ligand binding leads to dimerization and activation by sequential autophosphorylation on tyrosine residues. Inhibited by ARQ 069; this compound maintains the kinase in an inactive conformation and inhibits autophosphorylation. Inhibited by PD173074.
|Protein tissue specificity|| |
Detected in astrocytoma, neuroblastoma and adrenal cortex cell lines. Some isoforms are detected in foreskin fibroblast cell lines, however isoform 17, isoform 18 and isoform 19 are not detected in these cells.
|Involvement in disease|| |
Pfeiffer syndrome (PS) [MIM:101600]: A syndrome characterized by the association of craniosynostosis, broad and deviated thumbs and big toes, and partial syndactyly of the fingers and toes. Three subtypes are known: mild autosomal dominant form (type 1); cloverleaf skull, elbow ankylosis, early death, sporadic (type 2); craniosynostosis, early demise, sporadic (type 3). . Note: The disease is caused by mutations affecting the gene represented in this entry.; Hypogonadotropic hypogonadism 2 with or without anosmia (HH2) [MIM:147950]: A disorder characterized by absent or incomplete sexual maturation by the age of 18 years, in conjunction with low levels of circulating gonadotropins and testosterone and no other abnormalities of the hypothalamic-pituitary axis. In some cases, it is associated with non-reproductive phenotypes, such as anosmia, cleft palate, and sensorineural hearing loss. Anosmia or hyposmia is related to the absence or hypoplasia of the olfactory bulbs and tracts. Hypogonadism is due to deficiency in gonadotropin-releasing hormone and probably results from a failure of embryonic migration of gonadotropin-releasing hormone-synthesizing neurons. In the presence of anosmia, idiopathic hypogonadotropic hypogonadism is referred to as Kallmann syndrome, whereas in the presence of a normal sense of smell, it has been termed normosmic idiopathic hypogonadotropic hypogonadism (nIHH). . Note: The disease is caused by mutations affecting distinct genetic loci, including the gene represented in this entry. Some patients carrying mutations in FGFR1 also have a mutation other HH-associated genes including DUSP6, FGF8, FGF17, FLRT3, GNRH1, GNRHR, HS6ST1, IL17RD, ANOS1, KISS1R, NSMF, PROKR2, SPRY4 and TACR3 (PubMed:23643382). .; Osteoglophonic dysplasia (OGD) [MIM:166250]: Characterized by craniosynostosis, prominent supraorbital ridge, and depressed nasal bridge, as well as by rhizomelic dwarfism and nonossifying bone lesions. Inheritance is autosomal dominant. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Hartsfield syndrome (HRTFDS) [MIM:615465]: A syndrome characterized by the triad of holoprosencephaly, ectrodactyly, and cleft/lip palate. Profound mental retardation is also present. Multiple other congenital anomalies usually occur. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Trigonocephaly 1 (TRIGNO1) [MIM:190440]: A keel-shaped deformation of the forehead, caused by premature fusion of the metopic sutures. It results in a triangular shape of the head. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Note: A chromosomal aberration involving FGFR1 may be a cause of stem cell leukemia lymphoma syndrome (SCLL). Translocation t(8;13)(p11;q12) with ZMYM2. SCLL usually presents as lymphoblastic lymphoma in association with a myeloproliferative disorder, often accompanied by pronounced peripheral eosinophilia and/or prominent eosinophilic infiltrates in the affected bone marrow. .; Note: A chromosomal aberration involving FGFR1 may be a cause of stem cell myeloproliferative disorder (MPD). Translocation t(6;8)(q27;p11) with FGFR1OP. Insertion ins(12;8)(p11;p11p22) with FGFR1OP2. MPD is characterized by myeloid hyperplasia, eosinophilia and T-cell or B-cell lymphoblastic lymphoma. In general it progresses to acute myeloid leukemia. The fusion proteins FGFR1OP2-FGFR1, FGFR1OP-FGFR1 or FGFR1-FGFR1OP may exhibit constitutive kinase activity and be responsible for the transforming activity. .; Note: A chromosomal aberration involving FGFR1 may be a cause of stem cell myeloproliferative disorder (MPD). Translocation t(8;9)(p12;q33) with CNTRL. MPD is characterized by myeloid hyperplasia, eosinophilia and T-cell or B-cell lymphoblastic lymphoma. In general it progresses to acute myeloid leukemia. The fusion protein CNTRL-FGFR1 is found in the cytoplasm, exhibits constitutive kinase activity and may be responsible for the transforming activity.; Encephalocraniocutaneous lipomatosis (ECCL) [MIM:613001]: A sporadically occurring, neurocutaneous disorder characterized by ocular anomalies, skin lesions, and central nervous system anomalies. Clinical features include a well-demarcated hairless fatty nevus on the scalp, benign ocular tumors, intracranial and intraspinal lipomas, and congenital abnormalities of the meninges. Seizures, spasticity, and intellectual disability can be present. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Jackson-Weiss syndrome (JWS) [MIM:123150]: An autosomal dominant craniosynostosis syndrome characterized by craniofacial abnormalities and abnormality of the feet: broad great toes with medial deviation and tarsal-metatarsal coalescence. . Note: The disease is caused by mutations affecting the gene represented in this entry.
|Protein sequence and domain|| |
The second and third Ig-like domains directly interact with fibroblast growth factors (FGF) and heparan sulfate proteoglycans. Isoforms lacking the first Ig-like domain have higher affinity for fibroblast growth factors (FGF) and heparan sulfate proteoglycans than isoforms with all three Ig-like domains. / Belongs to the protein kinase superfamily. Tyr protein kinase family. Fibroblast growth factor receptor subfamily. / Contains 3 Ig-like C2-type (immunoglobulin-like) domains. / Contains 1 protein kinase domain.
|Protein post-translational modifications|| |
Autophosphorylated. Binding of FGF family members together with heparan sulfate proteoglycan or heparin promotes receptor dimerization and autophosphorylation on tyrosine residues. Autophosphorylation occurs in trans between the two FGFR molecules present in the dimer and proceeds in a highly ordered manner. Initial autophosphorylation at Tyr-653 increases the kinase activity by a factor of 50 to 100. After this, Tyr-583 becomes phosphorylated, followed by phosphorylation of Tyr-463, Tyr-766, Tyr-583 and Tyr-585. In a third stage, Tyr-654 is autophosphorylated, resulting in a further tenfold increase of kinase activity. Phosphotyrosine residues provide docking sites for interacting proteins and so are crucial for FGFR1 function and its regulation. / Ubiquitinated. FGFR1 is rapidly ubiquitinated by NEDD4 after autophosphorylation, leading to internalization and lysosomal degradation. CBL is recruited to activated FGFR1 via FRS2 and GRB2, and mediates ubiquitination and subsequent degradation of FGFR1. / N-glycosylated in the endoplasmic reticulum. The N-glycan chains undergo further maturation to an Endo H-resistant form in the Golgi apparatus.
|Protein cellular localization|| |
Cell membrane; Single-pass type I membrane protein / Nucleus / Cytoplasm > cytosol / Cytoplasmic vesicle
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St John’s Laboratory Ltd.
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