PLGF
- Known as:
- PLGF
- Catalog number:
- Y214368
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- PLGF
Ask about this productRelated genes to: PLGF
- Gene:
- PGF NIH gene
- Name:
- placental growth factor
- Previous symbol:
- PGFL
- Synonyms:
- PLGF, PlGF-2, PlGF, SHGC-10760, D12S1900, PIGF
- Chromosome:
- 14q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-14
- Date modifiied:
- 2016-05-20
Related products to: PLGF
Anti-human PlGF (#178 G10), Biotin, Source: Monoclonal Murine, MABAnti-human PlGF (#178/G10), Biotin, Source: Monoclonal Murine, MABAnti-human PlGF (#331 H12), Source: Monoclonal Murine, MABAnti-human PlGF (#331/H12), Source: Monoclonal Murine, MABAnti-human PlGF (AG) (nat.), Source: Polyclonal Rabbit, PABAnti-human PlGF (MAB), Source: Monoclonal Murine, MABAnti-human PlGF (Prot.A) (nat.), Source: Polyclonal Rabbit, PABAnti-human PlGF (Prot.A) (nat.), Source: Polyclonal Rabbit, PABAnti-human PlGF AntibodyAnti-human PlGF antibodyAnti-human PlGF, Source: Polyclonal Rabbit, PABAnti-human PlGF, Source: Polyclonal Rabbit, PABAnti-Human PlGF-1Anti-Human PlGF-1Anti-Human PlGF-1 Related articles to: PLGF
- Retinopathy is a common symptom in mitochondrial diseases, and a leading cause of blindness in working-age individuals, often arising as a consequence of diabetes. Here, we demonstrate that postnatal loss of the replicative helicase of mitochondrial DNA in the astrocytes and Müller glia induces neovascular retinopathy. In these retinas, the macroglia show pathological reactivation, leading to hallmark features of neovascularization with blood-retina-barrier leakage, secondary microgliosis, and complement cascade activation. Similar reactivation of astrocytes in the cerebral cortex does not compromise vascular integrity, indicating tissue-specific roles of mitochondrial metabolism in macroglia for vascular homeostasis. Three secreted angiogenic factors-Fgf2, Pgf, and Lcn2-known to contribute to diabetic retinopathy, were induced. Spike recordings of the most sensitive retinal ganglion cells revealed normal rod function and intact retinal coding. These findings highlight the critical role of glial mitochondrial metabolism in neovascular retinopathy, with important implications for therapy development for mitochondrial and common forms of vision loss. - Source: PubMed
Publication date: 2026/05/08
Olander SofiiaKaraman SinemSuomi FumiAguilar KevinZhaivoron AleksandraNedergaard MaikenSmeds LinaTiihonen JussiQuintana AlbertHidalgo JuanAlitalo KariAla-Laurila PetriInce-Dunn GulayseSuomalainen Anu - Maternal recognition of pregnancy (MRP) in cattle is dependent on embryonic signaling, including decreased synthesis of prostaglandin Fα (PGFα) and increased synthesis of prostaglandin E (PGE) and PGE:PGFα ratio, and elevated interferon tau (IFNT) expression factors essential for corpus luteum (CL) maintenance. PGE and PGFα are synthesized by the maternal endometrium and embryo trophoblastic cells. Fatty acids (FAs) are known to modulate prostaglandin (PG) biosynthesis, however, their effects on bovine trophoblastic cells (CT-1) remain unclear. This study aimed to investigate the effects of linoleic acid (LA), conjugated linoleic acid (CLA), oleic acid (OA), and a combination of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on PG production (PGE, PGFα, and PGE:PGFα ratio) and on transcripts related to PG synthesis (PTGS2, PTGES1, PTGES2, AKR1B1) and MRP signaling (PTGER4, IFNT, MMP2, and MMP9) in CT-1 cells. CT-1 cultures were treated with each FAs for 5 min, 24, 48, and 72 h. PGE and PGFα concentrations were measured by ELISA, and transcript abundance was assessed by RT-qPCR after 48 h for all groups, with IFNT also evaluated at 24 and 72 h in control and LA groups. LA significantly increased PGE at 24 (P < 0.00001), 48 (P < 0.00001), and 72 h (P = 0.0019) compared to other treatments, and elevated the PGE:PGFα ratio at 24 (P = 0.0102) and 48 h (P = 0.0032). Compared to the control group, LA upregulated PTGS2 (21.73 ± 1.55 vs. 12.51 ± 1.55; P = 0.0031) and PTGES2 (0.11 ± 0.01 vs. 0.07 ± 0.01; P = 0.0204) after 72 h, and increased IFNT expression at 24 (P = 0.0454) and 72 h (P = 0.0006). In conclusion, LA increases PGE synthesis and PGE2:PGF2α ratio, and alters expression of transcripts involved in PG synthesis and IFNT, indicating its potential modulator capable of favoring the MRP in cattle. - Source: PubMed
Publication date: 2026/04/30
Bezerra Lucas de OliveiraRolniche Laura Chuba MachadoMendes Adriano FelipeSilva Amanda Guimarães daFeltrin Isabella RioMorelli Karine GalhegoPrestes Catarina LazareviciusPinto Maria Eduarda RochaMaldonado Mariângela Bueno CordeiroRocha Cecilia ConstantinoEaly AlanMercadante VitorPugliesi GuilhermeMembrive Claudia Maria Bertan - Over the course of Parkinson's disease (PD), there is considerable intersubject variability in gray matter (GM) loss across a wide range of subcortical structures and cortical areas, which is often predictive of the clinical trajectory of the disease. The biological or clinical factors underlying these individual differences are not well understood. Obstructive sleep apnea (OSA) is a sleep-disordered breathing that is associated with an increased risk of cognitive impairment and neurodegeneration. In this study, we investigated whether moderate-to-severe OSA in untreated de novo PD is linked to more severe GM atrophy compared to PD without OSA and a group of controls. High-resolution structural 3 T MRI T1 and T2-weighted scans were used to estimate subcortical GM volumes and hippocampal subfields, and to perform vertex-wise analyses of cortical thickness and cortical surface area. We found that the presence of OSA was associated with a significant bilateral reduction in hippocampal volume, particularly in the CA1, CA3, and subicular regions, an effect specifically observed in PD patients and not in the control group. These findings suggest that the co-occurrence of OSA and PD may be related to early structural brain changes, highlighting the importance of timely OSA diagnosis and management to potentially delay cognitive decline in PD. - Source: PubMed
Publication date: 2026/05/05
Burdová KristínaRůžička FilipMana JosefFilip PavelNepožitek JiříDostálová SimonaPeřinová PavlaBezdicek OndrejGregorovič PetrHavlík FilipRůžička EvženDušek PetrŠonka KarelJech Robert - Breast carcinoma is a major cause of cancer-related mortality among women worldwide. Identifying novel molecular targets remains essential, particularly for aggressive triple-negative breast cancer (TNBC). Leucine-rich alpha-2-glycoprotein 1 (LRG1) has been linked to tumor progression and angiogenesis, but its molecular mechanisms in breast cancer are poorly defined. We evaluated the effects of recombinant human LRG1 (rhLRG1) on cell viability and migration in MDA-MB-231 TNBC cells and performed transcriptomic profiling followed by functional enrichment analyses using GenArise, Cytoscape, and R-based tools. RhLRG1 treatment significantly increased cell viability and migration. Transcriptomic analysis revealed activation of key oncogenic cascades, including the PI3K/AKT, MAPK, and RAS signaling pathways. Hub-gene analysis identified upregulated genes involved in proliferation (, , ), angiogenesis (, ), and apoptosis (, ), whereas downregulated genes were associated with apoptotic resistance (, ) and adhesion (, ). Functional enrichment highlighted LRG1's role in the bioinformatic analysis of differentially expressed genes that were obtained from microarray assays. LRG1 remodels the tumor microenvironment by promoting proliferation, angiogenesis, and apoptotic sensitivity while repressing resistance-related genes. These findings position LRG1 as a potential diagnostic biomarker and therapeutic target for advanced breast carcinoma. - Source: PubMed
Publication date: 2026/04/18
Osorio-Antonio FedericoDiaz-González Daniela MichelCampos-Viguri Gabriela ElizabethSánchez-López José ManuelCortez-Sánchez José LuisCastelán FranciscoChávez-Rios Jesús RamsesMaycotte-González PaolaCortés-Hernández PaulinaPeralta-Zaragoza OscarBautista-Rodríguez Elizabeth - The corpus luteum (CL) is essential for progesterone production and maintenance of early pregnancy in ruminants. Luteal function is critically influenced by the balance between prostaglandin E (PGE) and F (PGF), which is regulated by key synthases such as PTGES and PGFS. Interferon-tau (IFNT), the pregnancy recognition signal in ruminants, is known to modulate prostaglandin production. However, its precise role and underlying mechanisms in regulating PGE and PGF production within goat CL remain unclear. In this study, the expression of key prostaglandin synthases was progressively upregulated in the CL throughout early pregnancy (days 5-18), accompanied by an increase in the PTGES/PGFS ratio. In goat luteal cells, IFNT significantly increased PTGES expression without affecting PGFS, and elevated the PGE/PGF ratio. IFNT dose- and time-dependently induced ISG15 expression, and concurrently upregulated ISGylation-related enzymes. Notably, ISG15 overexpression recapitulated the effects of IFNT by selectively upregulating PTGES expression, thereby enhancing PGE production and the PGE/PGF ratio. Conversely, ISG15 knockdown attenuated the IFNT-induced effects. Further mechanistic investigations revealed that both conjugated and free forms of ISG15 contribute to the upregulation of PTGES and the subsequent increase in the PGE/PGF ratio. Collectively, these findings identify ISG15-mediated elevation of the PGE/PGF ratio as a key mechanism by which the pregnancy recognition signal IFNT protects the CL, providing new insights into the maintenance of early pregnancy in goats. - Source: PubMed
Publication date: 2026/04/21
Shang ChunmeiLiu HaokunLi ZuhuiMou YuanmengFan ChenlingLiu ShanJin YapingLin Pengfei