Anti_EphB1, EphB2, EphB3 Monoclonal
- Known as:
- Anti_EphB1, EphB2, EphB3 Monoclonal
- Catalog number:
- Y091058
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Anti_EphB1 EphB2 EphB3 Monoclonal
Related genes to: Anti_EphB1, EphB2, EphB3 Monoclonal
- Gene:
- EPHB2 NIH gene
- Name:
- EPH receptor B2
- Previous symbol:
- DRT, ERK, EPHT3
- Synonyms:
- Hek5, Tyro5
- Chromosome:
- 1p36.12
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-09
- Date modifiied:
- 2019-04-23
- Gene:
- EPHB3 NIH gene
- Name:
- EPH receptor B3
- Previous symbol:
- ETK2
- Synonyms:
- Hek2, Tyro6
- Chromosome:
- 3q27.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-07
- Date modifiied:
- 2015-09-11
Related products to: Anti_EphB1, EphB2, EphB3 Monoclonal
Related articles to: Anti_EphB1, EphB2, EphB3 Monoclonal
- Neuropathic pain after spinal cord injury reflects persistent hyperexcitability in the spinal cord dorsal horn, yet the molecular drivers sustaining this maladaptive state are unknown. Using an antibody microarray of dorsal horn tissue from mice six weeks after cervical contusion spinal cord injury, we found persistent upregulation of Eph-ephrin signaling, including increased EphB1, EphB2 and EphB3 expression and phosphorylation. Reversible chemogenetic inhibition of EphB kinase activity, using an EphB1/2/3 analog-sensitive knock-in mouse, selectively reversed established mechanical allodynia without affecting thermal hyperalgesia or motor function and also shifted dorsal horn signaling away from pain sensitization-associated pathways. Among EphB receptors, EphB2 showed the most consistent and robust injury-induced increase in expression within dorsal horn. Although EphB2 transcript levels increased in both dorsal horn neurons and astrocytes, conditional deletion of EphB2 only in dorsal horn neurons, but not in astrocytes, reversed established mechanical allodynia and reduced dorsal horn neuronal activation. These findings identify EphB signaling, and neuronal EphB2 in particular, as a mechanism that actively maintains pain hypersensitivity after spinal cord injury. - Source: PubMed
Publication date: 2026/04/22
Heinsinger Nicolette MJaffe David ASrikanth Kolluru DLyttle Megan ASmith Madison SThomas Samantha JCharsar Brittany ACheng LanMichel-Flutot PaulineCain Rachel EWatson Jaime LBao DuranFan JiaFalnikar AditiZhou WeiDalva Matthew BLepore Angelo C - The global prevalence of metabolic syndrome had created one of the most pressing public health dilemmas and significant financial burden to the healthcare system. Despite the surge of glucagon-like peptide-1 agonists, recent studies showed that 40 % of body weight loss is due to lean mass loss, raising the concern about induction of musculoskeletal arthritis. Therefore, there is an urgent need to develop novel therapeutic strategies to tackle the progression of metabolic disorders with minimal adverse effects. EphB singaling had been validated in the progression of metabolic syndrome. We leveraged the resolved X-ray crystal structure of the hEphB1 kinase domain to introduce thienopyridine-based analogs (termed STA analogs) that showed potential pan-inhibitory profiles for EphB1, EphB2, and EphB4 with no inhibition for EphB3 tyrosine kinase singaling pathways. STA-013 inhibited EphB1, EphB2, and EphB4 tyrosine kinases selectively, as validated by a premier kinase profiling assay against 140 protein kinases, with no inhibitory profile against EphB3 tyrosine kinase. Systemic injections of STA-013 resulted in weight loss with significant reduction of fat mass and perseverance of lean mass. This was associated with significant improvement in glucose homeostasis, mitigation of insulin resistance, and inhibition of fatty liver in high-fat diet-induced obese mice. This was allied with modulation of respiratory exchange rates during the dark cycle, with no change in food intake. Additionally, STA-013 administration resulted in inhibiting the EphB phosphorylated signal, coupled with increased p-AKT/AKT signaling, to suggest insulin signaling activation. STA-013 showed an elevated signal for InsR-β, which reversed the effect of insulin on InsR degradation, allowing for the restoration of glucose homeostasis and mitigating insulin resistance. - Source: PubMed
Publication date: 2025/08/05
Tareq SyedEwida Heba AZoubi SumaihBenson HarrisonPatel DhavalkumarDiab HaninPatra SouvikRedrovan DanielaNozohouri EhsanBassani Taysa BerivanCardoso Alisson CamposFrimpong-Manson KofiKhodavirdilou LidaAziz Md TareqWilkerson Jenny LThompson JonathanBickel UlrichChelikani Prasanth KFarag AymanAhmed Mahmoud Salama - This study aimed to investigate the developmental, macroscopic, microscopic and immunohistochemical characteristics of tongue tissues in sheep foetuses collected at three gestational periods. The study was carried out with foetuses collected from pregnant ewes slaughtered in private slaughterhouses. For this purpose, a total of 15 foetuses, 5 each from the first trimester (38-48 days), second trimester (56-73 days) and third trimester (105-118 days), were used. Foetal tongues were carefully dissected and removed from the oral cavity. First, their macroscopic properties were examined using a stereomicroscope. Scanning electron microscopy was used for microscopic morphological evaluations, and the tongues were examined under a light microscope using Haematoxylin Eosin and Masson Trichrome methods. The expression and localization of cytokeratins (CK)-5, E-cadherin, EphB2 and EphB3 proteins in the tongue epithelium were determined by immunohistochemical analysis. According to the results of light and electron microscopy, it was determined that the tongue tissue began to develop in the first trimester, and lingual papillae could be seen as primitive primordia. Although the tongue continued to grow in the second trimester, primitive taste buds and papilla structures were detected. In the last trimester, lingual papillae were observed to become more prominent. In addition to taste buds, serous glands in the papillae were also detected. It was determined that both taste and mechanical papillae formed simultaneously during the development of lingual papillae, and the papillae were located at the apex, body and root without a chronological order. Furthermore, epithelial markers such as CK-5 and E-cadherin as well as EphB2 and EphB3 receptor expressions were detected in the epithelium covering the papillae in all three trimesters. In addition to contributing to the morphological literature, our results may provide information for future studies aimed at elucidating the normal development of the tongue and other epithelial tissues in sheep. - Source: PubMed
Güzel Barış CanIşbilir İhsanYavaş Senem EsinIşbilir Fatma - Trauma-associated glioblastoma has been previously described, albeit without molecular characterization. - Source: PubMed
Publication date: 2025/05/19
Georgescu Maria-MagdalenaOlar AdrianaZollinger William Daniel - Spinal cord injury is a severe neurological condition with limited neuronal regeneration and functional recovery. Currently, no effective treatments exist to improve spinal cord injury prognosis. Neuronal guidance proteins are a diverse group of molecules that play crucial roles in axon and dendrite growth during nervous system development. Increasing evidence highlights their regulatory functions in spinal cord injury. This review provides a brief overview of the modulation patterns of key neuronal guidance proteins in neuronal axon growth during nervous system formation and subsequently focuses on their roles in neuronal regeneration and functional recovery following spinal cord injury. Neuronal guidance proteins include, but are not limited to, semaphorins and their receptors, plexins; netrins and their receptors, deleted in colorectal cancer and UNC5; Eph receptors and their ligands, ephrins; Slit and its receptor, Robo; repulsive guidance molecules and their receptor, neogenin; Wnt proteins and their receptor, Frizzled; and protocadherins. Localized Netrin-1 at the injury site inhibits motor axon regeneration after adult spinal cord injury while promoting oligodendrocyte growth. Slit2 enhances synapse formation in the injured spinal cord of rats. EphA7 regulates acute apoptosis in the early pathophysiological stages of spinal cord injury, while ephrinA1 plays a role in the nervous system's injury response, with its reduced expression leading to impaired motor function in rats. EphA3 is upregulated following spinal cord injury, promoting an inhibitory environment for axonal regeneration. After spinal cord injury, bidirectional activation of ephrinB2 and EphB2 in astrocytes and fibroblasts results in the formation of a dense astrocyte-meningeal fibroblast scar. EphB1/ephrinB1 signaling mediates pain processing in spinal cord injury by regulating calpain-1 and caspase-3 in neurons. EphB3 expression increases in white matter after spinal cord injury, further inhibiting axon regeneration. Sema3A, expressed by neurons and fibroblasts in the scar surrounding the injury, inhibits motor neuron and sensory nerve growth after spinal cord injury. Sema4D suppresses neuronal axon myelination and axon regeneration, while its inhibition significantly enhances axon regeneration and motor recovery. Sema7A is involved in glial scar formation and may influence serotonin channel remodeling, thereby affecting motor coordination. Given these findings, the local or systemic application of neuronal guidance proteins represents a promising avenue for spinal cord injury treatment. - Source: PubMed
Publication date: 2025/05/06
Tang LinyanSong ZhiWang JieHe ShenghuaLiu Chao