Overview

  • Product name
    Anti-NESP55 antibody
  • Description
    Rabbit polyclonal to NESP55
  • Tested applications
    Suitable for: ICC/IF, IHC-Pmore details
  • Species reactivity
    Reacts with: Human
  • Immunogen

    Recombinant fragment, corresponding to amino acids 121-226 of Human NESP55 (UniProt: O95467).

  • Positive control
    • Human pancreas tissue.

Properties

Applications

Our Abpromise guarantee covers the use of ab150798 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
ICC/IF Use a concentration of 1 - 4 µg/ml.

Recommend PFA Fixation and Triton X-100 treatment

IHC-P 1/1000 - 1/2500. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.

Target

  • Relevance
    Defects in GNAS are a cause of ACTH-independent macronodular adrenal hyperplasia (AIMAH); also known as adrenal Cushing syndrome due to AIMAH. A rare adrenal defect characterized by multiple, bilateral, non-pigmented, benign, adrenocortical nodules. It results in excessive production of cortisol leading to ACTH-independent Cushing syndrome. Clinical manifestations of Cushing syndrome include facial and trunkal obesity, abdominal striae, muscular weakness, osteoporosis, arterial hypertension, diabetes. Genetic variations in GNAS are the cause of pseudohypoparathyroidism type 1B (PHP1B). PHP1B is characterized by parathyroid hormone (PTH)-resistant hypocalcemia and hyperphosphatemia. Patients affected with PHP1B have normal activity of the product of GNAS, lack developmental defects characteristic of AHO, and typically show no other endocrine abnormalities besides resistance to PTH. Most affected individuals have defects in methylation of the gene. In some cases microdeletions involving the STX16 appear to cause loss of methylation at exon A/B of GNAS, resulting in PHP1B. Paternal uniparental isodisomy have also been observed. Defects in GNAS are the cause of GNAS hyperfunction (GNASHYP). This condition is characterized by increased trauma-related bleeding tendency, prolonged bleeding time, brachydactyly and mental retardation. Both the XLas isoforms and the ALEX protein are mutated which strongly reduces the interaction between them and this may allow unimpeded activation of the XLas isoforms.
  • Cellular localization
    Cytoplasmic vesicle, secretory vesicle (By similarity). Secreted
  • Database links
  • Alternative names
    • adenylate cyclase-stimulating G alpha protein antibody
    • AHO antibody
    • alpha stimulating activity polypeptide 1 antibody
    • Alternative gene product encoded by XL-exon antibody
    • C20orf45 antibody
    • extra large alphas protein antibody
    • GNAS antibody
    • GNAS1 antibody
    • GPSA antibody
    • GSP antibody
    • guanine nucleotide binding protein (G protein) antibody
    • guanine nucleotide regulatory protein antibody
    • guanine nucleotide-binding protein G(s) subunit alpha isoforms XLas antibody
    • NESP antibody
    • Neuroendocrine secretory protein 55 antibody
    • neuroendocrine secretory protein antibody
    • PHP1A antibody
    • PHP1B antibody
    • PHP1C antibody
    • POH antibody
    • protein ALEX antibody
    • RP4-543J19.4 antibody
    • secretogranin VI antibody
    see all

Images

  • Immunofluorescent staining of Human cell line U-2 OS shows positivity in nucleus but not nucleoli. Recommended concentration of ab150798 1-4 µg/ml. Cells treated with PFA/Triton X-100.
  • Immunohistochemical analysis of paraffin embedded Human pancreas tissue labeling NESP55 with ab150798 at a dilution of 1/1000.

References

ab150798 has not yet been referenced specifically in any publications.

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Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"

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