Adipo R1{adiponectin receptor 1}rabbit.pAb
- Known as:
- Adipo R1{adiponectin receptor 1}host: rabbit.pAb
- Catalog number:
- 201-20-7142
- Product Quantity:
- 0.1ml
- Category:
- -
- Supplier:
- Shanghai Sunred
- Gene target:
- Adipo R1{adiponectin receptor 1}rabbit.pAb
Related genes to: Adipo R1{adiponectin receptor 1}rabbit.pAb
- Gene:
- ADIPOQ NIH gene
- Name:
- adiponectin, C1Q and collagen domain containing
- Previous symbol:
- ACDC
- Synonyms:
- ACRP30, AdipoQ, apM1, GBP28, adiponectin
- Chromosome:
- 3q27.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-26
- Date modifiied:
- 2016-10-05
Related products to: Adipo R1{adiponectin receptor 1}rabbit.pAb
guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) polyclonal antibody"Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP"(Ala1)-PAR-4 (1-6) (mouse)
(Ala1)-Thrombin Receptor-Like 3 (1-6) (mouse), (Ala1)-Proteinase Activated Receptor 4 (1-6) (mouse), (Ala1)-Coagulation Factor II Receptor-Like 3 (1-6) (mouse), AYPGKF 98%(Ala1)-PAR-4 (1-6) amide (mouse)
AYPGKFamide, (Ala1)-Thrombin Receptor-Like 3 (1-6) amide (mouse), (Ala1)-Coagulation Factor II Receptor-Like 3 (1-6) amide (mouse), (Ala1)-Proteinase Activated Recepto(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II Related articles to: Adipo R1{adiponectin receptor 1}rabbit.pAb
- Inter-organ communication is governed by a complex "secretome," yet mapping the journey of these factors from their origin to precise cellular destinations remains a fundamental challenge. Proximity labeling emerges as a powerful tool to dissect the secretome, yet conventional workflows typically rely on single-compartment biotinylation at the endoplasmic reticulum (ER), failing to capture proteins that utilize unconventional secretion. Here, we present DuO-SCOUT (Dual-Organelle Secretome Conjugation and Organ-Uptake Tracking), a high-performance platform that simultaneously targets BioID2 to the ER and the trans-Golgi network (TGN). This integrated strategy captures the full secretory maturation relay, increasing protein identification by over 120% compared to traditional ER-anchored methods. We translated this in vivo using an Adipoq-Cre mouse model to map the adipose secretome. To bridge the gap between systemic transport and tissue-specific uptake, DuO-SCOUT integrates BSPA (Biotin-Specific Proximity Amplification), a visualization toolkit detecting biotinylated proteins with sub-nanomolar sensitivity. In obese mice, we identified the piriform cortex (PIR) as a previously unrecognized extra-hypothalamic sink for adipose-derived leptin. This is associated with a localized neuroinflammatory signature, including significant induction of Il6. DuO-SCOUT establishes a broadly applicable framework for dissecting the complex molecular logic of systemic organ-organ communication. - Source: PubMed
Publication date: 2026/08/14
Yang FenglianQian RuiSong JiaxingMeng XingqiKim Jin YoungLai Kwok OnWang LiZhang Liang - Type 2 diabetes (T2D) is a multifactorial disorder arising from complex interactions between genetic susceptibility and environmental exposures, including diet. This systematic review aimed to synthesize and critically evaluate evidence on gene-diet interactions in T2D-related phenotypes among adults without diagnosed T2D at baseline. - Source: PubMed
Publication date: 2026/07/26
Kapellou AngelikiPapailia SevastianiFotis ThanasisVrachnos Dimitrios MiltiadisPapageorgiou DimitriosSalata EffieNtoumou EleniVittas Spiros - Exhaustion of skeletal stem and progenitor cells (SSPCs) drives age-related delays in fracture repair, yet the upstream regulators of SSPC maintenance are unclear. We identify that core-binding factor β (Cbfβ) in bone marrow Adipoq cells (BMACs) is essential for maintaining SSPC number and function. Cbfβ deletion in BMACs (CKO) leads to SSPC depletion, including periosteal populations, and impairs bicortical fracture healing in mice. Multi-omics (RNA-seq, CUT&Tag-seq, and ATAC-seq) reveal that Cbfβ preserves chromatin accessibility at DNA repair loci, maintaining genomic stability, preventing BMAC senescence, and mitigating the senescence-associated secretory phenotype (SASP). Senolytic therapy alleviates BMAC senescence, restores SSPC populations, and improves bone repair in CKO mice. In both humans and mice, Cbfβ expression declines with aging, accompanied by increased BMAC senescence. AAV-mediated Cbfβ overexpression restores aging-related bone repair and SSPC decline. These findings reveal a novel mechanism in which Cbfβ in BMACs regulates SSPC maintenance via a senescence/SASP axis, offering a potential therapeutic strategy for age-related bone repair deficits. - Source: PubMed
Publication date: 2026/08/10
Huang TiannanWu ShaliQian WeiChen RuiyingChen ErmanWang MeizhuZhang CuiZhou ChenheYu LuyangWu MengjieLi Yi-PingWu Mengrui - Adipokines play an important role in metabolism, insulin sensitivity, and inflammation, and may provide distinct contributions to the pathophysiology of type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). The differences in roles of the adiponectin-leptin ratio (ALR), visfatin, and tumor necrosis factor-alpha (TNF-α) in the various subtypes of diabetes are still not fully understood. This cross-sectional study involved 141 participants, divided into healthy controls (n = 47), patients with T1DM (n = 47), and patients with T2DM (n = 47). Serum adiponectin, leptin, visfatin, TNF-α, fasting plasma glucose (FPG), glycated hemoglobin (HbA1c), and serum insulin levels were measured. The ALR was calculated. Insulin resistance and β-cell function were examined using homeostasis model assessment (HOMA) indices. We performed group comparisons, correlation studies, logistic regression tests, and receiver operating characteristic (ROC) curve analyses. The differences observed were all statistically significant. Participants with T2DM showed a more adverse metabolic profile, characterized by greater waist circumference and higher levels of FPG, HbA1c, serum insulin, leptin, and TNF-α, along with lower levels of adiponectin and ALR. Participants with T1DM also exhibited altered adipokine profiles compared to controls, notably with increased levels of leptin and TNF-α. All diabetic groups had decreased levels of visfatin, with the T2DM group showing the largest reduction. ROC analysis demonstrated effective discrimination of TNF-α, ALR, and visfatin in this group. This study highlights the different inflammatory and adipokine profiles across diabetes subtypes. The assessment of these biomarkers enhances the understanding of metabolic differences between T1DM and T2DM. However, these findings are exploratory and require validation in large, controlled studies. - Source: PubMed
Publication date: 2026/07/22
Wu BoHe HuixiangZeng JinlongLai XiaoliBai Yan - and are genes encoding membrane progestin receptor αand β (mPRα and mPRβ, respectively), which are currently classified as members of the progestin and adipoQ receptor (PAQR) family. For mPRα, the first identified mPR gene, there are two paralogs in zebrafish, and . In order to elucidate the physiological functions of the mPR subtypes, we created gene knockout (KO) fish by editing seven genes in zebrafish and analyzing their phenotypes. The null-mutant strains of , , and presented no significant abnormalities in reproductive functions. Thus, we generated a triple-gene knockout (TKO) strain of these highly related genes. The TKO strain had reduced fecundity and a high percentage of abnormal embryos. The embryos exhibited various types of abnormal morphology. In histological sections, a reduction in the number of nucleoli in germinal vesicles was observed. Additionally, the distribution of the nucleolus was abnormal. The amount of 18S and 28S ribosomal RNAs in the oocytes significantly increased. These analyses indicate that , , and are responsible for the production of the nucleolus, which is necessary for supplying the proper number of ribosomal RNAs into the cytoplasm of oocytes. Abnormal embryo development resulted from low-quality eggs in TKO zebrafish, suggesting that , , and mutations affect oogenesis. These results indicate that Paqr7a, Paqr7b, and Paqr8 are required for the preparation of the nucleolus during oogenesis. Insufficient formation of the nucleolus resulted in a higher quantity of ribosomal RNA in the cytoplasm, causing abnormal embryo development. - Source: PubMed
Farid Md AlmamunTanvir Md RazainMouri TakumiTsutsumi EiseiRahman Sohan Md SohanurHasan Md EkramulRahman Md SaydurYamamoto ChihiroMaeno AkiteruTokumoto Toshinobu