EPHB1 (+ EPHB2 + 3 + 4) antibody Host rabbit
- Known as:
- EPHB1 (+ EPHB2 + 3 + 4) (anti-) Host host: rabbit
- Catalog number:
- 'B8098-2
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- EPHB1 (+ EPHB2 + 3 4) antibody Host rabbit
Related genes to: EPHB1 (+ EPHB2 + 3 + 4) antibody Host rabbit
- Gene:
- EPHB1 NIH gene
- Name:
- EPH receptor B1
- Previous symbol:
- EPHT2
- Synonyms:
- Hek6
- Chromosome:
- 3q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-03-23
- Date modifiied:
- 2016-01-15
- 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
Related products to: EPHB1 (+ EPHB2 + 3 + 4) antibody Host rabbit
Related articles to: EPHB1 (+ EPHB2 + 3 + 4) antibody Host rabbit
- 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 - Eph receptors and Ephrin ligands are a large highly conserved family of interacting membrane-anchored molecules that form dimers, tetramers, and tetramer superclusters to become activated and signal upon cell-cell contact. While most noted for their ability to transduce bidirectional phosphotyrosine signals in development, certain Ephs and Ephrins also become overexpressed and participate in pathological situations, including EphB1 in chronic pain/addiction and EphB2 in fibroinflammatory disorders and cancer. We searched for small molecules that disrupt EphB-EphrinB receptor-ligand interactions and discovered compounds with submicromolar activity that specifically inhibit formation of the tetramer. Compounds effectively target tetramer-driven EphB1-EphrinB2 and EphB2-EphrinB2 interactions, while showing less action towards the more dimer-driven EphB4-EphrinB2 interaction. They are orally available, exhibit drug-like qualities to reduce both EphB forward and EphrinB reverse signaling, and act to blunt inflammatory pain and opioid withdrawal behaviors. Tetramer inhibitors thus present a novel way to target Eph-Ephrin macromolecular interactions and counter pathologies caused or exacerbated by excessive bidirectional signaling. - Source: PubMed
Publication date: 2025/12/25
Wang HanghangKhambete AmavSprouse FrancesKarsi MelodyCortez KarinaBellinghausen EricKhuu TamdanBlock NatalieTalebian AsgharAhmed Mahmoud SalamaGedara Mahesh UdamulleOrtiz MichaelHenkemeyer Mark - 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 - 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