Key features and details
- Rabbit polyclonal to Ret (phospho Y1062)
- Suitable for: IHC-P, WB
- Reacts with: Human
- Isotype: IgG
Product nameAnti-Ret (phospho Y1062) antibody
See all Ret primary antibodies
DescriptionRabbit polyclonal to Ret (phospho Y1062)
Specificityab51103 detects endogenous levels of Ret only when phosphorylated at tyrosine 1062.
Tested applicationsSuitable for: IHC-P, WBmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse, Rat
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Storage instructionsShipped at 4°C. Store at -20°C. Stable for 12 months at -20°C.
Storage bufferpH: 7.40
Preservative: 0.02% Sodium azide
Constituents: 50% Glycerol, 0.87% Sodium chloride, PBS
Without Mg+2 and Ca+2
Concentration information loading...
PurityImmunogen affinity purified
Purification notesab51103 was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific phosphopeptide. The antibody against non-phosphopeptide was removed by chromatography using non-phosphopeptide corresponding to the phosphorylation site.
Our Abpromise guarantee covers the use of ab51103 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-P||Use at an assay dependent concentration.|
|WB||1/500 - 1/1000. Predicted molecular weight: 124 kDa.|
FunctionProbable receptor with tyrosine-protein kinase activity; important for development.
Involvement in diseaseDefects in RET may be a cause of colorectal cancer (CRC) [MIM:114500].
Defects in RET are a cause of Hirschsprung disease (HSCR) [MIM:142623]. HSCR is a genetic disorder of neural crest development characterized by the absence of intramural ganglion cells in the hindgut, often resulting in intestinal obstruction. Occasionally, MEN2A or FMTC occur in association with HSCR.
Defects in RET are the cause of medullary thyroid carcinoma (MTC) [MIM:155240]. MTC is a rare tumor derived from the C cells of the thyroid. Three hereditary forms are known, that are transmitted in an autosomal dominant fashion: (a) multiple neoplasia type 2A (MEN2A), (b) multiple neoplasia type IIB (MEN2B) and (c) familial MTC (FMTC), which occurs in 25-30% of MTC cases and where MTC is the only clinical manifestation.
Defects in RET are the cause of multiple neoplasia type 2B (MEN2B) [MIM:162300]. MEN2B is an uncommon inherited cancer syndrome characterized by predisposition to MTC and phaeochromocytoma which is associated with marfanoid habitus, mucosal neuromas, skeletal and ophtalmic abnormalities, and ganglioneuromas of the intestine tract. Then the disease progresses rapidly with the development of metastatic MTC and a pheochromocytome in 50% of cases.
Defects in RET are a cause of susceptibility to pheochromocytoma (PCC) [MIM:171300]. A catecholamine-producing tumor of chromaffin tissue of the adrenal medulla or sympathetic paraganglia. The cardinal symptom, reflecting the increased secretion of epinephrine and norepinephrine, is hypertension, which may be persistent or intermittent.
Defects in RET are the cause of multiple neoplasia type 2A (MEN2A) [MIM:171400]; also known as multiple neoplasia type 2 (MEN2). MEN2A is the most frequent form of medullary thyroid cancer (MTC). It is an inherited cancer syndrome characterized by MTC, phaeochromocytoma and/or hyperparathyroidism.
Defects in RET are a cause of thyroid papillary carcinoma (TPC) [MIM:188550]. TPC is a common tumor of the thyroid that typically arises as an irregular, solid or cystic mass from otherwise normal thyroid tissue. Papillary carcinomas are malignant neoplasm characterized by the formation of numerous, irregular, finger-like projections of fibrous stroma that is covered with a surface layer of neoplastic epithelial cells. Note=Chromosomal aberrations involving RET are found in thyroid papillary carcinomas. Inversion inv(10)(q11.2;q21) generates the RET/CCDC6 (PTC1) oncogene; inversion inv(10)(q11.2;q11.2) generates the RET/NCOA4 (PTC3) oncogene; translocation t(10;14)(q11;q32) with GOLGA5 generates the RET/GOLGA5 (PTC5) oncogene; translocation t(8;10)(p21.3;q11.2) with PCM1 generates the PCM1/RET fusion; translocation t(6;10)(p21.3;q11.2) with RFP generates the Delta RFP/RET oncogene; translocation t(1;10)(p13;q11) with TRIM33 generates the TRIM33/RET (PTC7) oncogene; translocation t(7;10)(q32;q11) with TRIM24/TIF1 generates the TRIM24/RET (PTC6) oncogene. The PTC5 oncogene has been found in 2 cases of PACT in children exposed to radioactive fallout after Chernobyl. A chromosomal aberration involving TRIM27/RFP is found in thyroid papillary carcinomas. Translocation t(6;10)(p21.3;q11.2) with RET. The translocation generates TRIM27/RET and delta TRIM27/RET oncogenes.
Defects in RET are a cause of renal adysplasia (RADYS) [MIM:191830]; also known as renal agenesis or renal aplasia. Renal agenesis refers to the absence of one (unilateral) or both (bilateral) kidneys at birth. Bilateral renal agenesis belongs to a group of perinatally lethal renal diseases, including severe bilateral renal dysplasia, unilateral renal agenesis with contralateral dysplasia and severe obstructive uropathy.
Defects in RET are a cause of congenital central hypoventilation syndrome (CCHS) [MIM:209880]; also known as congenital failure of autonomic control or Ondine curse. CCHS is a rare disorder characterized by abnormal control of respiration in the absence of neuromuscular or lung disease, or an identifiable brain stem lesion. A deficiency in autonomic control of respiration results in inadequate or negligible ventilatory and arousal responses to hypercapnia and hypoxemia.
Sequence similaritiesBelongs to the protein kinase superfamily. Tyr protein kinase family.
Contains 1 cadherin domain.
Contains 1 protein kinase domain.
modificationsAutophosphorylated on C-terminal tyrosine residues upon ligand stimulation. Dephosphorylated by PTPRJ on Tyr-905, Tyr-1015 and Tyr-1062.
- Information by UniProt
- C ret antibody
- Cadherin family member 12 antibody
- Cadherin related family member 16 antibody
All lanes : Anti-Ret (phospho Y1062) antibody (ab51103) at 1/500 dilution
Lane 1 : K562 cell lysate.
Lane 2 : K562 cell Lysate. For this panel, ab51103 was pre-incubated with immunizing peptide.
Predicted band size: 124 kDa
Ab51103 staining human normal testis tissue. Staining is localised to cell membranes.
Left panel: with primary antibody at 1 ug/ml. Right panel: isotype control.
Sections were stained using an automated system (DAKO Autostainer Plus), at room temperature: sections were rehydrated and antigen retrieved with the Dako 3 in 1 AR buffer EDTA pH 9.0 in a DAKO PT Link. Slides were peroxidase blocked in 3% H2O2 in methanol for 10 mins. They were then blocked with Dako Protein block for 10 minutes (containing casein 0.25% in PBS) then incubated with primary antibody for 20 min and detected with Dako envision flex amplification kit for 30 minutes. Colorimetric detection was completed with Diaminobenzidine for 5 minutes. Slides were counterstained with Haematoxylin and coverslipped under DePeX. Please note that for manual staining we recommend to optimize the primary antibody concentration and incubation time (overnight incubation), and amplification may be required.
ab51103 has been referenced in 6 publications.
- Wang H et al. YAP confers resistance to vandetanib in medullary thyroid cancer. Biochem Cell Biol 98:443-448 (2020). PubMed: 32449862
- Han Y et al. Tumor-Induced Generation of Splenic Erythroblast-like Ter-Cells Promotes Tumor Progression. Cell 173:634-648.e12 (2018). PubMed: 29606356
- Pozo K et al. Preclinical characterization of tyrosine kinase inhibitor-based targeted therapies for neuroendocrine thyroid cancer. Oncotarget 9:37662-37675 (2018). PubMed: 30701022
- Franz H et al. The histone code reader SPIN1 controls RET signaling in liposarcoma. Oncotarget 6:4773-89 (2015). WB . PubMed: 25749382
- Kang CW et al. Antitumor Activity and Acquired Resistance Mechanism of Dovitinib (TKI258) in RET-Rearranged Lung Adenocarcinoma. Mol Cancer Ther 14:2238-48 (2015). PubMed: 26208525
- He S et al. GFRa1 released by nerves enhances cancer cell perineural invasion through GDNF-RET signaling. Proc Natl Acad Sci U S A 111:E2008-17 (2014). ICC/IF . PubMed: 24778213