Leptin receptor overlapping transcript-like 1 (LEPROTL1)

The protein contains 131 amino acids for an estimated molecular weight of 14428 Da.

 

Negatively regulates growth hormone (GH) receptor cell surface expression in liver. May play a role in liver resistance to GH during periods of reduced nutrient availability. (updated: Sept. 12, 2018)

Protein identification was indicated in the following studies:

  1. D'Alessandro and co-workers. (2017) Red blood cell proteomics update: is there more to discover? Blood Transfus. 15(2), 182-187.

Methods

The following articles were analysed to gather the proteome content of erythrocytes.

The gene or protein list provided in the studies were processed using the ID mapping API of Uniprot in September 2018. The number of proteins identified and mapped without ambiguity in these studies is indicated below.
Only Swiss-Prot entries (reviewed) were considered for protein evidence assignation.

PublicationIdentification 1Uniprot mapping 2Not mapped /
Obsolete
TrEMBLSwiss-Prot
Goodman (2013)2289 (gene list)227853205992269
Lange (2014)123412347281224
Hegedus (2015)2638262202352387
Wilson (2016)165815281702911068
d'Alessandro (2017)18261817201815
Bryk (2017)20902060101081942
Chu (2018)18531804553621387

1 as available in the article and/or in supplementary material
2 uniprot mapping returns all protein isoforms as one entry

The compilation of older studies can be retrieved from the Red Blood Cell Collection database.

The data and differentiation stages presented below come from the proteomic study and analysis performed by our partners of the GReX consortium, more details are available in their published work.

No sequence conservation computed yet.

This protein is predicted to be membranous by TOPCONS.


Interpro domains
Total structural coverage: 98%
Model score: 0
No model available.

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No binding partner found

The reference OMIM entry for this protein is 607338

Leptin receptor overlapping transcript-like 1; leprotl1

CLONING

Huang et al. (2001) identified LEPROTL1 by randomly sequencing clones obtained from a fetal brain cDNA library. The deduced 131-amino acid integral membrane protein has an external N terminus, an internal C terminus, and 3 transmembrane domains. It also contains a potential JAK2 (147796) phosphorylation site. LEPROTL1 shares 67% identity with a leptin receptor (601007) gene-related protein (OBRGRP, or LEPROT; 613461). Northern blot analysis revealed expression of a 2.9-kb main transcript in almost all tissues examined. Highest expression was detected in heart, testis, adrenal gland, thymus, and spleen, and lowest expression was detected in lung and skeletal muscle. Several transcripts were detected in some tissues, notably testis.

GENE FUNCTION

During periods of reduced nutrient availability, the liver becomes resistant to the action of growth hormone (GH1; 139250). Touvier et al. (2009) found that transgenic mice expressing human LEPROT or LEPROTL1 became growth retarded and that their isolated hepatocytes showed reduced GH-binding capacity and impaired GH-dependent cell signaling. Transgenic mice expressing both LEPROT and LEPROTL1 showed a more severe phenotype and significantly reduced expression of GH-dependent genes. In contrast, knockdown of Leprot or Leprotl1 in a rat hepatocyte cell line elevated GH-binding capacity and GH-dependent cell signaling. Hepatic Leprot and Leprotl1 mRNA expression was increased in mice by fasting and streptozoticin-induced diabetes, whereas insulin treatment of cultured rat hepatocytes had the opposite effect. Touvier et al. (2009) concluded that LEPROT and LEPROTL1 influence liver GH signaling and are involved in nutritional signals, body growth, and metabolism.

MAPPING

By radiation hybrid analysis, Huang et al. (2001) mapped the LEPROTL1 gene to chromosome 8p21.2-p21.1. ... More on the omim web site

Subscribe to this protein entry history

June 30, 2020: Protein entry updated
Automatic update: OMIM entry 607338 was added.

Oct. 19, 2018: Additional information
Initial protein addition to the database. This entry was referenced in Bryk and co-workers. (2017).