MW 411.9 Da, Purity >98%. Highly potent, selective, competitive, non-peptide CCK1 receptor antagonist (Ki = 0.2 nM). Increases plasma leptin levels. Shows central effects. Stimulates food intake *in vivo.* Orally active.
1 25 dihydroxyvitamin D3 receptor, 25-dihydroxyvitamin D3 receptor, AP-1, Activator protein 1, BXR, CCK A, CCK-A receptor, CCK1-R, CCKAR_HUMAN, CCKR Type A, CCKRA, Cholecystokinin A receptor, Cholecystokinin receptor type A, Cholecystokinin type A receptor, Cholecystokinin-1 receptor, Deubiquitinating enzyme 1, Enhancer Binding Protein AP1, JUN protein, JUNC, JUN_HUMAN, Jun Activation Domain Binding Protein, Jun oncogene, Jun proto oncogene, Member 1, NF-E2-related factor 2, NF2L2_HUMAN, NR1C3, NR1I1, NR1I2_HUMAN, NRF2, Nfe2l2, Nuclear factor, Nuclear factor (erythroid derived 2) like 2, Nuclear factor erythroid 2-related factor 2, Nuclear factor erythroid derived 2 like 2, Nuclear receptor subfamily 1 group C member 3, Nuclear receptor subfamily 1 group I member 1, Nuclear receptor subfamily 1 group I member 2, ONR 1, OTTHUMP00000215173, OTTHUMP00000215174, OTTHUMP00000215175, Oncogene JUN, Orphan nuclear receptor PAR 1, Orphan nuclear receptor PXR, PAR, PAR q, PPAR-gamma, PPARG2, PPARG_HUMAN, PPP1R163, PRR, Peroxisome proliferator activated receptor gamma 2, Peroxisome proliferator-activated receptor gamma, Pregnane X receptor, Protein phosphatase 1, regulatory subunit 163, Proto-oncogene c-jun, SXR, Steroid and xenobiotic receptor, TRFR_HUMAN, TRH Receptor, TRH-R, Thyroliberin receptor, Thyrotropin-releasing hormone receptor, Transcription factor AP-1, UBP, UBP1_HUMAN, Ubiquitin carboxyl-terminal hydrolase 1, Ubiquitin specific peptidase 1, Ubiquitin specific protease 1, Ubiquitin thioesterase 1, Ubiquitin thiolesterase 1, Ubiquitin-specific-processing protease 1, V jun sarcoma virus 17 oncogene homolog, V jun sarcoma virus 17 oncogene homolog (avian), V-jun avian sarcoma virus 17 oncogene homolog, VDR_HUMAN, Vitamin D (1,25- dihydroxyvitamin D3) receptor, Vitamin D hormone receptor, Vitamin D nuclear receptor variant 1, Vitamin D receptor, Vitamin D3 receptor, cJun, erythroid derived 2, hUBP, like 2, nuclear factor erythroid 2 like 2, p39, pregnane X nuclear receptor variant 2
MW 411.9 Da, Purity >98%. Highly potent, selective, competitive, non-peptide CCK1 receptor antagonist (Ki = 0.2 nM). Increases plasma leptin levels. Shows central effects. Stimulates food intake *in vivo.* Orally active.
Soluble in DMSO to 100 mM.
Highly potent, selective, competitive, non-peptide CCK1 receptor antagonist (Ki = 0.2 nM). Increases plasma leptin levels. Shows central effects. Stimulates food intake *in vivo.* Orally active.
The c-Jun protein also known as AP-1 is a transcription factor with a molecular weight of approximately 39 kDa. It is widely expressed in various tissues particularly in neurons where it plays a role in gene regulation. Vitamin D Receptor (VDR) a nuclear receptor of about 48 kDa binds with vitamin D to regulate calcium homeostasis and is mainly found in the intestines bones and kidneys. PPAR gamma 2 involved in adipocyte differentiation weighs around 57 kDa and expresses mainly in adipose tissue. The Pregnane X Receptor (PXR) approximately 50 kDa is a nuclear receptor found in the liver and small intestine important for xenobiotic metabolism. TRH-R or thyrotropin-releasing hormone receptor and CCK1-R or cholecystokinin receptor are membrane-bound receptors involved in hormone signaling primarily in the central nervous system and gastrointestinal tract. USP1 is an ubiquitin-specific protease critical for protein degradation pathways frequently found in proliferating cells. Lastly Nrf2 acts as a regulator of antioxidant proteins and expresses in many cell types under stress conditions.
These proteins influence substantial aspects of cellular function and metabolism. c-Jun forms part of the AP-1 complex impacting cellular proliferation and apoptosis. Vitamin D Receptor modulates gene expression related to immune responses and bone development. PPAR gamma 2 influences fat storage and glucose metabolism. PXR regulates the expression of enzymes involved in drug metabolism. TRH-R and CCK1-R transmit signals essential for hormone-mediated physiological responses. USP1 contributes to DNA repair and maintaining genomic stability. Nrf2 when activated translocates to the nucleus to initiate the transcription of antioxidant response genes working alongside enzymes such as HO-1.
These proteins integrate into significant metabolic and regulatory networks. c-Jun influences the MAPK signaling pathway associating closely with proteins like JNK. Vitamin D Receptor plays an important role in the calcium signaling pathway and interacts with retinoid X receptors. PPAR gamma 2 aligns with adipogenesis pathways and cross-talks with insulin signaling. PXR integrates into the detoxification pathway often synergizing with cytochrome P450 enzymes. TRH-R and CCK1-R operate within the neuroendocrine signaling pathways. USP1 functions within the DNA damage response pathway working with PCNA and FANCD2. Nrf2 is principally involved in the oxidative stress pathway collaborating with proteins like KEAP1.
These proteins have strong links to various health conditions. Dysfunctional c-Jun activity associates with neurodegenerative diseases including Alzheimer's as it affects neuron survival. Vitamin D Receptor impairment connects to bone disorders like rickets. PPAR gamma 2 mutations can result in metabolic syndromes such as diabetes linked with insulin resistance proteins. PXR variations might influence susceptibility to liver diseases through altered metabolism. Abnormal TRH-R and CCK1-R signaling can contribute to psychiatric disorders and digestive problems respectively. USP1 mutations are associated with cancer given its role in genomic stability. Aberrant Nrf2 function connects to chronic inflammatory conditions by altering stress response pathways.
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