KDELR2: A GPCR Receptor Involved in Cellular Signaling and Cellular Processes

Target Name: KDELR2

NCBI ID: G11014

KDELR2

KDELR2: A GPCR Receptor Involved in Cellular Signaling and Cellular Processes

KDELR2 (Kirsten dual-specificity modifier of ELL-1 and Leucine-rich repeat-containing G protein-coupled receptor 2) is a protein that is expressed in various tissues and cells in the body. It is a member of the G protein-coupled receptor (GPCR) family, which is a large superfamily of transmembrane proteins that play a critical role in cellular signaling. GPCRs are involved in a wide range of physiological processes, including sensory perception, neurotransmitter signaling, and hormone regulation.

KDELR2 is a 21-kDa protein that is expressed in the brain, heart, skeletal muscles, and other tissues. It is localized to the endoplasmic reticulum (ER) and the nuclear envelope (NE), which are both protein-rich organelles that play important roles in the regulation of intracellular signaling pathways. KDELR2 is highly conserved, with a calculated pI of 6.9 and a predicted localization in the cell membrane.

KDELR2 is involved in a wide range of cellular signaling pathways, including those that regulate sensory perception, neurotransmitter signaling, and hormone regulation. It is a critical regulator of the neurotransmitter GABA, which is a key modulator of brain activity and a well-known neurotransmitter Involved in anxiety, depression, and other neurological disorders.

KDELR2 is also involved in the regulation of ion channels, which are critical for the rapid and efficient transmission of electrical signals through the cell membrane. The KDELR2 channel is a GPCR that is involved in the regulation of neuronal excitability, and it is thought to play a role in the pathophysiology of epilepsy and other neurological disorders.

In addition to its role in neurotransmission, KDELR2 is also involved in the regulation of cellular signaling pathways that are critical for cell survival and proliferation. It is a regulator of the cell survival signaling pathway, which is involved in the regulation of cell cycle progression and apoptosis.

KDELR2 is also involved in the regulation of inflammation, which is a critical aspect of cellular signaling that is involved in the regulation of immune responses and the regulation of inflammation. It is a regulator of the transcription factor Nrf2, which is involved in the regulation of gene expression and is thought to play a key role in the regulation of cellular signaling pathways that are involved in inflammation.

KDELR2 is also involved in the regulation of pain perception, which is a critical aspect of cellular signaling that is involved in the regulation of pain sensitivity and the regulation of neurotransmission. It is a regulator of the nociceptin receptor, which is involved in the regulation of pain perception and is thought to play a key role in the pathophysiology of pain disorders.

In conclusion, KDELR2 is a protein that is involved in a wide range of cellular signaling pathways that are critical for the regulation of intracellular signaling, cell survival, and inflammation. Based on its conserved structure and the wide range of cellular processes that it is involved in, KDELR2 is a promising drug target and a potential biomarker for a variety of neurological and psychiatric disorders.

Protein Name: KDEL Endoplasmic Reticulum Protein Retention Receptor 2

Functions: Membrane receptor that binds the K-D-E-L sequence motif in the C-terminal part of endoplasmic reticulum resident proteins and maintains their localization in that compartment by participating to their vesicle-mediated recycling back from the Golgi (PubMed:1325562, PubMed:18086916, PubMed:33053334). Binding is pH dependent, and is optimal at pH 5-5.4 (By similarity)

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•   general information;
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•   protein biological mechanisms;
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•   the target screening and validation;
•   expression level;
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•   pharmacochemistry experiments;
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The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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