Cited by 88Cellular transport and secretionReceptor Mechanisms and SignalingAdrenal Hormones and Disorders

Failed export of the adrenocorticotrophin receptor from the endoplasmic reticulum in non-adrenal cells: evidence in support of a requirement for a specific adrenal accessory factor

Open access
Noon, LA, Franklin, JM, King, PJ, Goulding, NJ, Hunyady, L, Clark, AJ·2002·Journal of Endocrinology

Abstract

Difficulty in expressing the adrenocorticotrophin (ACTH) receptor (melanocortin 2 receptor; MC2R) after transfection of various MC2R expression vectors has been experienced by many researchers. Reproducible evidence for expression has been obtained only in the Y6/OS3 corticoadrenal cell lines or in cells expressing endogenous melanocortin receptors. In order to determine the cause of this failure of expression we have undertaken the following studies. An MC2R expression plasmid was constructed in which the green fluorescent protein (GFP) coding region had been added to the C-terminus of the mature protein. Transfection of this plasmid into Y6 cells with a cAMP-responsive reporter plasmid demonstrated normal function of this receptor. Imaging of CHO cells expressing MC2R-GFP revealed perinuclear expression, although a cholecystokinin receptor (CCKR)-GFP construct was efficiently expressed at the cell surface. Y6 cells, in contrast, showed cell surface fluorescence after transfection with MC2R-GFP. Several other cell types showed a similar pattern of GFP distribution characteristic of retention in the endoplasmic reticulum. Counterstaining with an anti-KDEL antibody confirmed this location. Co-expression of the MC2R and the CCKR-GFP did not impair CCKR trafficking to the cell surface, implying a receptor-specific impairment to trafficking in the CHO cell which was absent in the Y6 cell.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1677/joe.0.1740017

Cites

44 of 44 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • MC2R cannot function alone as an ACTH receptor.

    “The MC2R cannot function alone as an ACTH receptor, which led to many difficulties in its characterization after initial cloning (33).”

    From ACTH Antagonists (2016) · cites this paper as [33]

    The Introduction and Discussion report that MC2R was difficult to characterize after cloning because functional expression was difficult to obtain in non-adrenal cells. The Discussion hypothesizes that MC2R requires an accessory factor for expression, but does not establish the categorical claim that it cannot function alone as an ACTH receptor. Page numbers were not available in our copy. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Noon, L., Franklin, J., King, P., Goulding, N., Hunyady, L., & Clark, A.
Affiliations
  • University of London (GB)
  • Semmelweis University (HU)
Corresponding author
Clark, AJ
Venue
Journal of Endocrinology
Published
2002-07-01
Volume
174
Issue
1
Pages
17-25
ISSN
  • 0022-0795 (ISSN-L)
  • 1479-6805
OpenAlex
W2106099541
Cited by
88
References
44
Citations by year
2026: 1 · 2025: 3 · 2023: 5 · 2022: 5 · 2021: 2 · 2020: 1 · 2019: 4 · 2017: 5 · 2016: 4 · 2015: 2 · 2014: 8 · 2013: 4 · 2012: 1
FWCI
1.58
Type
journal article
Language
en
Open access
Locations
  • Journal of Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Queen Mary University of London
  • University of Toronto
  • National Institutes of Health
  • National Institute of Diabetes and Digestive and Kidney Diseases
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
Keywords
melanocortin 2 receptor, endoplasmic reticulum retention, receptor trafficking, KDEL, cholecystokinin receptors, GFP fusion constructs, CHO cells
MeSH terms
Adrenocorticotropic Hormone, Animals, Endoplasmic Reticulum, Cricetinae, Luminescent Proteins, Receptors, Cholecystokinin, Transfection, Blotting, Western, CHO Cells, Receptors, Corticotropin, Receptor, Melanocortin, Type 2, Green Fluorescent Proteins

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review