Human Polyclonal BMP7 Ab
- Known as:
- Human Polyclonal BMP7 Antibody
- Catalog number:
- a0723
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal BMP7
Related genes to: Human Polyclonal BMP7 Ab
- Gene:
- BMP7 NIH gene
- Name:
- bone morphogenetic protein 7
- Previous symbol:
- -
- Synonyms:
- OP-1
- Chromosome:
- 20q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-05
- Date modifiied:
- 2016-10-05
Related products to: Human Polyclonal BMP7 Ab
Related articles to: Human Polyclonal BMP7 Ab
- Bone morphogenetic proteins (BMPs) are bone-derived osteokines that regulate energy metabolism and combat obesity by promoting brown adipocyte differentiation. BMP4, BMP7, BMP8B, and BMP9 are highly expressed in osteoblasts and bone matrix, from which they are released into circulation. They act as endocrine factors that induce brown adipogenesis, increase mitochondrial biogenesis, and increase thermogenesis via conserved signaling pathways (Smad, MAPK, and PGC1α). Concurrently, these BMPs maintain skeletal homeostasis and mediate crosstalk between bone and metabolic organs, including adipose tissue and the hypothalamus, thereby regulating appetite and energy balance. Preclinical studies have confirmed that BMP-based interventions can increase energy expenditure, improve insulin sensitivity, and alleviate obesity-related complications. However, clinical translation remains hindered by adverse effects, short half-lives, and obesity-induced BMP resistance. This review first elucidates the peripheral and central regulatory mechanisms of BMPs in energy metabolism, clarifies the subtype-specific metabolic effects of major BMPs, further evaluates their therapeutic potential against obesity and metabolic syndrome, and finally analyzes the core obstacles to clinical implementation and corresponding solution strategies. - Source: PubMed
Publication date: 2026/06/18
Zhang JingJiang NanWang Li-JuanCao Ting-BingXie Yang-LiLi Li - The liver is known to play a pivotal role in modulating blood glucose homeostasis through intrahepatic glucose metabolism. Here, we reveal a unique mechanism by which fatty liver exacerbates hyperglycemia through remote communication from hepatocytes to intestinal stem cells (ISCs), independent of enhanced intrahepatic gluconeogenesis. Mechanistically, hepatocyte-derived alkaline phosphatase (ALP) targets α2δ-1 in ISCs to promote the membrane translocation of Ca1.2. This process triggers increased intracellular calcium levels, which subsequently activates the calcineurin/NFATC2 signaling axis, thereby inhibiting SOX21 expression. Then, decreased expression of SOX21 downregulated bone morphogenetic protein 7 (BMP7), ultimately hindering ISCs differentiation into intestinal L-cells. Consequently, the levels of hypoglycemic enteroendocrine hormones secreted by L-cells are decreased, thereby promoting hyperglycemia. Therapeutically, inhibiting ALP synthesis in fatty liver independently reduces blood glucose and synergistically enhances the hypoglycemic effect of metformin. Our study highlights the role of liver-gut communication in regulating the fate of ISC differentiation and blood glucose homeostasis. - Source: PubMed
Publication date: 2026/06/17
Ye JinbaoWan QianyiLiu XingzhuDeng YawenZhang ZehongChen HaiouGao ChaoxinZhang ShiyuZhu YuedanYan JinhuaYuan YuChen YiChen Haiyang - Adipose tissue has emerged as a dynamic endocrine organ that coordinates systemic energy balance and cardiometabolic health. This Review highlights the dual humoral and neuronal pathways through which adipose tissue regulates systemic metabolism. Humoral signals include peptide hormones, lipid mediators, metabolites, chemokines and exosomal microRNAs secreted by adipose depots. Neuronal circuits control adipose function rapidly and precisely: sympathetic efferents trigger lipolysis in white adipose tissue and thermogenesis in brown adipose tissue, whereas sensory afferents detect chemical, thermal and mechanical signals to adjust sympathetic activity. Nutritional and environmental stimuli (for example, diet, cold exposure and exercise), along with pathological states (for example, obesity, type 2 diabetes mellitus, lipodystrophy and ageing-associated disorders), dynamically modulate these endocrine and neural outputs. Methodological innovations, such as omics based on mass spectrometry or liquid chromatography-mass spectrometry, secretome labelling, adipose tissue organoid models and click chemistry, enable high-resolution characterization of adipose-derived signals and their targets. Finally, we discuss translational opportunities, including synthetic analogues of lipophilic hormones, and future therapeutic strategies that harness adipose communication networks. - Source: PubMed
Publication date: 2026/06/12
Tsuji TadatakaTseng Yu-Hua - Chordin is a cysteine-rich protein which acts as a regulator of bone morphogenetic protein (BMP) signalling in the extracellular matrix. Acting in concert with twisted gastrulation (TWSG1), chordin works as an antagonist of BMP signalling by binding tightly to the growth factor and is a vital component of the network of interactions that establish developmental signalling gradients. Chordin is known to interact with BMP ligands via its four von-Willebrand factor type C domains, but the function of the large central four CHRD domains were previously unknown. Here we show that these domains interact strongly with sulphated glycosaminoglycans (GAGs) and provide evidence for the location of the binding site using X-ray crystallographic analysis combined with mutagenesis and biophysical techniques. Additionally, we report the first recombinant expression and purification of the complete functional chordin, TWSG1, BMP2, BMP7 complex which was used to demonstrate that the four CHRD domains are largely redundant with respect to the role of chordin as an inhibitor of BMP ligands. We therefore propose that the four CHRD domains of chordin have relevance in the diffusion and localisation of chordin-TWSG1-BMP complexes at the tissue and organismal level, mediated by their interaction with GAGs or proteoglycans. - Source: PubMed
Publication date: 2026/06/12
Snee MatthewBirchenough Holly LBecker Mark HPopplewell Jonathan FAshe Hilary LBaldock Clair - Two recombinant bone morphogenetic proteins (BMP-2 and BMP-7) have received FDA approval for bone-related therapies. However, their clinical performance is limited by high costs, the need for supraphysiological doses, and adverse side effects. Here, we describe a chemically modified mRNA (cmRNA) encoding BMP-7 that promotes osteogenesis and functional ossification. The BMP-7 cmRNA is delivered using optimized lipid vectors and a composite fibrin-calcium phosphate scaffold. Among several lipids evaluated, two previously unexplored lipids efficiently condense mRNA and mediate its delivery. Transfer of BMP-7 cmRNA lipoplexes to human mesenchymal stromal cells activates intracellular vesicle transport and cytoskeletal remodeling, and regulates extracellular matrix production and calcium-associated processes. These responses were accompanied by robust mineralization and activation of key osteogenic pathways. , BMP-7 mRNA-activated scaffolds promote the formation of ossified tissue, with the highest dose yielding the largest ectopic bony growth. We further observe concurrent angiogenesis and neurogenesis, demonstrating coordinated tissue regeneration. This platform enables effective mRNA delivery for bone healing and can be applied to other tissues, facilitating the development of mRNA therapeutics in regenerative medicine. - Source: PubMed
Publication date: 2026/05/29
Del Toro Runzer ClaudiaRoumans NadiaBouwman Freek GPereira Herrera BetzabethCillero-Pastor BertaRoque MicaelaAmédée JoëlleBovine Elisede Groot Florence BarrèrePlank ChristianBanfi Andreadi Maggio Nunziavan Griensven MartijnBalmayor Elizabeth R