BDNF Recombinant Protein
- Known as:
- BDNF Recombinant Protein
- Catalog number:
- ZR-40-514
- Product Quantity:
- 0.01 mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- BDNF Recombinant Protein
Related genes to: BDNF Recombinant Protein
- Gene:
- BDNF NIH gene
- Name:
- brain derived neurotrophic factor
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11p14.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-01-15
- Date modifiied:
- 2016-06-01
- Gene:
- BDNF-AS NIH gene
- Name:
- BDNF antisense RNA
- Previous symbol:
- BDNFOS
- Synonyms:
- BT2A, BT2B, BT2C, BT2D, NCRNA00049, BDNF-AS1, BDNFAS
- Chromosome:
- 11p14.1
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2005-02-01
- Date modifiied:
- 2017-08-09
Related products to: BDNF Recombinant Protein
Related articles to: BDNF Recombinant Protein
- Brain-derived neurotrophic factor (BDNF) is widely recognized as a critical molecule for the survival, growth, and maintenance of neurons in both the central and peripheral nervous systems, as well as for the development of cognitive abilities and emotions. However, recent studies have shown that, in addition to its role as a universal brain "fertilizer", BDNF acts as a metabotrophin linking neuronal signaling with systemic metabolism. BDNF serves as a key factor that integrates the body's response to stress, physical activity, and food intake with cellular mechanisms underlying neural plasticity and normal brain function. The review presents evidence supporting BDNF as a bidirectionally metabolic "bridge": body metabolism controls BDNF production in the brain, while brain BDNF regulates body metabolism. Disruption of this regulatory axis is associated with a broad range of neurological and somatic disorders, as well as their comorbidities. Cellular mechanisms associated with disruptions in BDNF functions are explored in detail through the example of alcohol dependence, a condition characterized by both impaired brain signaling and somatic pathologies accompanied by metabolic changes. - Source: PubMed
Peregud Danil IGulyaeva Nataliya V - Chronic l-methionine (l-met) treatment induces hyperhomocysteinemia, which impairs neurogenesis and memory by increasing oxidative stress. Caffeic acid (CA) possesses antioxidant properties that reduce brain oxidative damage and promote neurogenesis. This study investigated the neuroprotective effects of caffeic acid against the impact of l-met on hippocampal neurogenesis. Forty male Sprague-Dawley rats were randomly assigned to four groups ( = 10 per group): Control, l-met, CA, and CA+l-met. Rats received daily oral gavage of l-met (1.7 g/kg) and/or CA (40 mg/kg) for 28 days. The results demonstrated that CA ameliorated l-met-induced decreases in DCX and Sox-2-positive cells in the SGZ of the dentate gyrus, as shown by immunofluorescence staining. CA also reversed the l-met-induced decreases in hippocampal protein expression of Nrf2, Sox-2, and BDNF, as determined by Western blotting. Furthermore, CA alleviated l-met-induced oxidative damage and decreased antioxidant enzyme activity in the prefrontal cortex (PF) and hippocampus. These findings demonstrate CA's ability to counteract neurotoxicity induced by l-methionine. - Source: PubMed
Publication date: 2026/05/30
Dornlakorn OabnithiSirichoat ApiwatPannangrong WanassananSritawan NatayaAranarochana AnusaraPrajit RamWigmore PeterWelbat Jariya Umka - Cervical cancer (CC) remains a significant threat to global public health, with high incidence and mortality rates. Understanding the molecular mechanisms governing CC progression is critical for developing novel diagnostic and therapeutic strategies. microRNAs (miRNAs) have emerged as important regulators in cancer biology. This study aimed to identify and characterize a miRNA involved in CC development to assess and its potential as a diagnostic and prognostic biomarker through integrative bioinformatic and experimental analyses. - Source: PubMed
Antaño-Arias RamónTorres-Rojas Francisco IsraelCampos-Viguri Gabriela ElizabethArizmendi-Izazaga AdánOrtiz-Ortiz JulioDircio-Maldonado RobertoAlarcón-Millán JuditBartolo-Ángel Fredy DavidFiallo-Rodríguez AlejandroJiménez-Wences HildaSalmerón-Bárcenas Eric Genaro - Cell therapy is a potential therapeutic choice to treatment spinal cord injure (SCI). Studies proved that hypoxic precondition has protective effects on damaged cells. It sounds that a sub-lethal hypoxic exposure is likely enhance survival rates of transplanted cells. The aim of this study is the effect a novel strategy of preconditioning of human dental pulp stem cells (hDPSCs) via hydrogen peroxide (HO) on treatment rat SCI model. The hDPSCs were isolated from human third molar. The cells were cultured in various concentrations of HO(0-400 μM) at different time points (2-48 hours). Then, the cell viability was estimated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. In rat SCI model, 0.5×10 hDPSCs with and without HO preconditioning were locally transplanted in contusion site. Behavioral assessment was rendered within 7 weeks after injection. Besides, the brain-derived neurotrophic factor (BDNF) was evaluated. The results of MTT showed that the cell viability rates were significantly lower at the higher concentrations of HO at various times. However, the cell viability declined, followed by exposure to 50 μM HO for a period of 2-12 hours compared with untreated cells. Basso, Beattie, and Bresnahan (BBB) findings revealed transplantation of the preconditioned hDPSCs increased BBB score significantly compared to the SCI group. Also, BDNF as a neurotrophic factor, dramatically increased in treated group. These finding suggest transplantation of sub-lethal concentration of HO preconditioned hDPSCs would have protective roles through paracrine signals by enhancing survival capability transplanted cells which can cause motor neuron recovery in SCI. - Source: PubMed
Publication date: 2026/05/28
Bojnordi Maryam NazmBagheri-Mohammadi SaeidHamidabadi Hatef Ghasemi - Chronic unpredictable mild stress (CUMS) is a validated model of anxiety- and depression-like disorders and is associated with impaired neuroplasticity. Dysregulation of the plasminogen activator system, particularly elevated plasminogen activator inhibitor-1 (PAI-1), may disrupt tissue plasminogen activator (tPA)-dependent brain-derived neurotrophic factor (BDNF) signaling and contribute to stress-induced behavioral deficits. However, the therapeutic relevance of PAI-1 inhibition in mood disorders remains poorly defined. - Source: PubMed
Publication date: 2026/05/22
Bahi AmineDreyer Jean-Luc