RHOBTB1 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- RHOBTB1 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100518
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- RHOBTB1 antibody Polyclonal Antibodies Primary antibodies
Related genes to: RHOBTB1 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- RHOBTB1 NIH gene
- Name:
- Rho related BTB domain containing 1
- Previous symbol:
- -
- Synonyms:
- KIAA0740
- Chromosome:
- 10q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-06-21
- Date modifiied:
- 2019-04-10
Related products to: RHOBTB1 antibody Polyclonal Antibodies Primary antibodies
Related articles to: RHOBTB1 antibody Polyclonal Antibodies Primary antibodies
- The RhoBTB1-Cullin3 (CUL3) pathway in smooth muscle cells (SMCs) controls the ubiquitination and proteasomal degradation of target proteins that regulate vasodilation, vasoconstriction, and the actin cytoskeleton, and through this blood pressure (BP) and arterial stiffness. Using proximity labelling coupled with mass spectrometry in A7R5 SMCs, we identified proteins which bound to the C-terminal half of RhoBTB1 which functions as an adapter to deliver substrates to CUL3. We examined the physiological relevance of one of these substrates, RbFox2. Co-immunoprecipitation validated the interaction of RbFox2 with RhoBTB1. RbFox2 expression was elevated in response to inhibition of the ubiquitination-proteasomal pathway, CUL3-deficiency, and RhoBTB1 inhibition by either siRNA or angiotensin II (ANG). RbFox2 was ubiquitinated in a RhoBTB1- and CUL3-dependent manner suggesting its regulation through the RhoBTB1-CUL3-dependent ubiquitin-proteasome pathway. Inhibition of RbFox2 impaired the actin cytoskeleton in A7R5 cells and in primary SMC from RbFox2Flox/Flox (RbFox2F/F) mice and decreased the levels of globular and filamentous actin. ANG increased BP and arterial stiffness of RbFox2F/F mice, but the progression of arterial stiffness was halted after SMC-specific RbFox2 deletion despite a continued rise in BP. We conclude that RhoBTB1 and RbFox2 are important regulators of arterial stiffness through a mechanism that influences cytoskeletal integrity. - Source: PubMed
Publication date: 2026/04/02
Kumar GauravChaihongsa NisitaBrozoski Daniel TGolosova DariaVazirabad IbrahimLu Ko-TingWackman Kelsey KSingh Ravi KSigmund Curt D - Pork is a major source of animal protein for humans, and as living standards have improved, consumer demand has shifted from quantity to quality. Amino acid and fatty acid compositions determine the nutritional value and flavor of pork. However, the genetic mechanisms underlying variation in these parameters have not been fully elucidated. In this study, we quantified 17 amino acids and 42 fatty acids in the muscle from three crossbred pig populations, namely Yorkshire × Tibetan (YT), Yorkshire × Neijiang (YN), and Duroc × Tibetan (DT). YT and YN pigs exhibited higher amino acid concentrations, while DT pigs showed elevated fatty acid levels. Subsequently, whole-genome resequencing of 73 pigs identified 24,125,658 high-quality SNPs, among which 146 were significantly associated with fatty acid traits, leading to the identification of 19 candidate genes linked to palmitic acid (i.e., , and ), oleic acid (i.e., , and ), and total fatty acids (i.e., ). Functional annotation revealed that these candidate genes participate primarily in pathways related to lipid metabolism, glucose homeostasis, and energy balance. The identified SNPs and candidate genes provide valuable insights into the genetic architecture of the fatty acid composition in pork and may serve as molecular targets for improving meat quality through breeding. - Source: PubMed
Publication date: 2026/01/29
Tang JieLiang YanAn RuiLuo GanTao XuanLiu PengliangGu Yiren - Osteoclasts and foreign body giant cells (FBGCs) are multinucleated cells derived from monocytes, but they have distinct functions. Osteoclasts resorb bone while FBGCs form in response to foreign material. Regarding bone implants, osteoclasts are responsible for implant integration, but also for bone resorption associated to implant loosening, while FBGCs play a role in the immune response to the foreign material. Little is known about which proteins in the local environment fine-tune the multinucleation of osteoclasts or FBGCs. One candidate is Activin A (ActA). It has been shown to induce larger, more active osteoclasts, but its effect on FBGC differentiation is unknown. We investigated the effect of ActA on the differentiation of osteoclasts and FBGCs from human CD14-positive monocytes. The number of multinucleated cells and the cell area was measured. qPCR was performed to assess the effect of ActA on gene expression. ActA's influence on osteoclast and FBGC formation was studied on plastic, bone and hydroxyapatite coated Titanium discs (ALD-HA). ActA induced fewer, but bigger and more active osteoclasts on plastic and bone. In contrast, ActA did not have an effect on FBGC number. On ALD-HA, ActA reduced the number of FBGCs, but did not influence osteoclast numbers. qPCR showed that ActA upregulated the expression of several genes such as TRAcP, CIITA, OLR1, RHOBTB1 and ALK4, but mainly in osteoclasts. These results show that ActA has a different effect on osteoclasts compared to FBGCs. This difference could be caused by a difference in the expression in the canonical ActA receptor ALK4. - Source: PubMed
Publication date: 2026/02/04
Kylmäoja ElinaKauppinen SamiAbushahba FalehFinnilä MikkoRitala MikkoLehenkari PetriTuukkanen Juhade Vries Teun JSchoenmaker Ton - ICH, a severe stroke, causes neuronal death, neuroinflammation, and cerebral edema due to mitochondrial and immune dysfunction. The molecular mechanisms of secondary brain injuries are unclear, limiting effective therapies. This study used bioinformatics and experiments to explore miR-940's role in ICH. MitoDEGs were identified via MitoCarta 3.0, and key miRNAs predicted using TargetScan and miRDB. A collagenase-induced ICH rat model with antagomir knockdown was used for validation. Neuronal damage, mitochondrial proteins, and immune cell dynamics were assessed using histopathology, qRT-PCR, Western blotting, and flow cytometry. Bioinformatics identified seven MitoDEGs and miR-940. Functional analysis linked them to mitochondrial metabolism and neuroinflammation. Inhibiting miR-940 in vivo reduced neuronal apoptosis and cerebral edema, and reversed RHOBTB1 and BCL2A1 dysregulation. Immune profiling showed increased monocyte/NK cell infiltration and decreased T/B lymphocytes in ICH, correlating with MitoDEGs. Flow cytometry confirmed miR-940's role in restoring T/B cell homeostasis, and Western blotting validated key MitoDEG expression changes. This study establishes miR-940 as a key regulator of mitochondrial-immune crosstalk in ICH, modulating neuronal survival and immune microenvironment remodeling. The identified MitoDEGs and miR-940 axis may serve as potential diagnostic and therapeutic targets for ICH. - Source: PubMed
Publication date: 2025/11/26
Zhao XingPingWan HaoFangLin BingyingLou Inmaculada XuXie ShangfuGuo JianWenWan HaiTongZhou Huifen - Diminished ovarian reserve (DOR) is associated with heightened risk of infertility, premature menopause, and various long-term health issues. Our previous research demonstrated a correlation between prenatal propylparaben exposure and DOR in F1 mice. Here, we further reveal that the DOR phenotypes can be transgenerationally inherited in F1-F3 mice, manifested through increased follicular atresia and decreased anti-Müllerian hormone levels. Excessive apoptosis of granulosa cells is found to underlie these pathological processes. By combining diverse sequencing techniques, we identify persistent Rhobtb1 hypomethylation across multiple generations. Further exploration reveals that RhoBTB1 regulates FGF18 via ubiquitination, triggering MAPK pathway activation and subsequent granulosa cell apoptosis. Notably, similar Rhobtb1 hypomethylation patterns are observed in blood samples from DOR patients. Furthermore, intervention with a methyl-donor diet effectively ameliorates DOR phenotypes in F1-F3 offspring. These findings highlight the transgenerational effects of DOR, elucidate its underlying causes and pathogenic mechanisms, and propose potential epigenetic therapy strategies. - Source: PubMed
Publication date: 2025/09/16
Li MiluWu YalingWei SitingZhang TianyuYan WeiGao YueyueChen YingyingHu DianxingWu TongLi MoWang WenwenLi YanZhou SuHe XimiaoWang ShixuanZhang Jinjin