PKM2 Blocking Peptide
- Known as:
- PKM2 Blocking Peptide
- Catalog number:
- 33r-3786
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- PKM2 Blocking Peptide
Related genes to: PKM2 Blocking Peptide
- Gene:
- PKM NIH gene
- Name:
- pyruvate kinase M1/2
- Previous symbol:
- PKM2
- Synonyms:
- THBP1, OIP3, PK3
- Chromosome:
- 15q23
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2017-09-15
Related products to: PKM2 Blocking Peptide
Related articles to: PKM2 Blocking Peptide
- Hypoxia poses a serious threat to aquatic organisms, yet the regulatory roles of non-coding RNAs, particularly the competing endogenous RNA (ceRNA) network, in fish under hypoxic stress remain poorly understood. In this study, we conducted whole-transcriptome sequencing of yellow catfish (Pelteobagrus fulvidraco) liver tissue under hypoxic conditions to systematically identify hypoxia-responsive lncRNAs and miRNAs and construct a comprehensive ceRNA network. A total of 14 differentially expressed lncRNAs (DElncs) and 112 miRNAs (DEmiRs) were identified. Functional enrichment analysis revealed that the target genes of DElncs were significantly involved in mitochondrial membrane permeability, energy metabolism, and the HIF-1 and mTOR signaling pathways, while those of DEmiRs were enriched in MAPK, calcium, and ErbB signaling pathways. Furthermore, we identified 22 DEmiRs commonly regulated under both hypoxic and hypoxic-bacterial dual stresses, representing core regulators of environmental adaptation. By integrating expression correlation and target prediction, we constructed the first lncRNA-miRNA-mRNA ceRNA network in hypoxic yellow catfish, comprising 5 DElncs, 11 DEmiRs, and 17 ceDETGs. Within this network, lnc162 (significantly down-regulated) and lnc1375 (markedly up-regulated) may act to regulate key apoptotic and metabolic genes such as fosb, sgk1, pkm, and hopx by sponging specific miRNAs, as predicted by our ceRNA analysis. These results reveal that lncRNAs mediate hypoxic adaptation by coordinating apoptosis and metabolic reprogramming via ceRNA mechanisms. Our study provides novel insights into the molecular basis of hypoxia tolerance in teleosts and offers potential genetic targets for breeding hypoxia-resistant fish strains. - Source: PubMed
Publication date: 2026/04/26
Han BingShi YaxuanLiu XinsheTao YifanQiang JunYin ShaowuNing Xianhui - Right ventricular failure (RVF) is the major cause of mortality in pulmonary arterial hypertension (PAH), and even mild inflammatory stress can precipitate rapid decompensation. Here we report that the long noncoding RNA TCONS_00052110 (TCONS) is upregulated in the right ventricle (RV) under inflammatory stress and may modulate stress-associated responses. In adult male Sprague-Dawley rats with monocrotaline-induced PAH, a low-dose lipopolysaccharide challenge precipitated acute RVF. Mechanistically, TCONS physically associates with polypyrimidine tract-binding protein 1 (PTBP1) and is associated with a prolonged PTBP1 protein half-life, consistent with reduced PTBP1 protein turnover. Elevated PTBP1 skews pyruvate kinase muscle (PKM) isoforms toward PKM2, favoring a PKM2-dominant metabolic state consistent with glycolysis-related remodeling. These changes are accompanied by mitochondrial injury and cytosolic cytochrome c release in vivo and in vitro. Using a cardiomyocyte-enriched AAV9-cTnT strategy, knockdown of TCONS was associated with normalization of the PKM2/PKM1 balance, attenuation of mitochondrial injury, preservation of RV functional indices after inflammatory challenge, and improved survival. Reanalysis of patient-derived datasets from PAH lung tissue and RV tissue spanning compensation-to-decompensation revealed enrichment of inflammatory and glycolysis-related pathways concordant with the TCONS-PTBP1 axis, supporting contextual relevance. These findings support a model of a post-transcriptional link between inflammatory stress, glycolysis-related remodeling, and mitochondrial injury in PAH-related RVF, warranting validation in human RV tissue. - Source: PubMed
Publication date: 2026/04/29
Gao XiaoweiYang YueGuo LizheWang LuQian LiQin GangLuo HuiCao YananWang E - We report findings on risk and resilience factors related to depression, their associations and combined interactions among older adolescents (15-19 years) living in urban slums in India. - Source: PubMed
Publication date: 2026/04/27
Daniel MercianPrashad LokenderKaur AmanpreetKallakuri SudhaDevarapalli SiddhardhaPaslawar SrilathaVishwakarma GayatriSagar RajeshMaulik Pallab Kumar - - Source: PubMed
Publication date: 2026/04/28
Xu DebinYu JichunYang YutingDu YunyanLu HongchengZhang ShouhuaFeng QianYu YiHao LiangShao JunChen Leifeng - Natural products are biologically active compounds used for therapeutic interventions for various diseases, particularly infections. Autophagy is an intracellular catabolic pathway involving lysosomal degradation and is closely associated with immunological pathways, effectively combating bacterial, viral, fungal, and parasitic infections. Accumulating evidence suggests that autophagy activation or inhibition by natural products promotes antimicrobial responses against various pathogens. Numerous natural products can modulate autophagy through diverse signaling pathways, suggesting their potential as a host-directed therapeutic strategy that may complement conventional drug regimens or help mitigate drug resistance in various infectious diseases. However, it remains largely unclear whether these effects are mediated by direct modulation of autophagy or indirectly through associated mechanisms, including enhanced immune defense, attenuation of pathological inflammation, or crosstalk with other organelle functions. Additionally, multiple pathogens can evade host responses; thus, autophagy activation may inadvertently create favorable conditions for certain pathogens. This review discusses the current knowledge of natural products in terms of their antimicrobial actions through autophagy regulation, particularly the roles of distinct natural product classes, such as polyphenols, alkaloids, terpenoids, quinones, peptides, and macrolides in modulating autophagy for potentially contributing to control various infectious diseases. Exploring the intricate molecular interplay between natural products and autophagy in limiting infections may provide valuable insights that could inform the development of innovative host-directed antimicrobial treatments based on autophagy regulation. 3-MA: 3-methyladenine; AM: alveolar macrophages; AMP: antimicrobial peptides; AMPK: 5' adenosine monophosphate-activated protein kinase; ARDS: acute respiratory distress syndrome; ART: artemisinin; ASFV: African swine fever virus; ATG: autophagy related; AZM: azithromycin; BafA1: bafilomycin A; BECN1: beclin 1; BMDM: bone marrow-derived macrophage; BNIP3: BCL2 interacting protein 3; BNIP3L: BCL2 interacting protein 3 like; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; CAMKK2: calcium/calmodulin-dependent protein kinase kinase 2; CBD: cannabidiol; CF: cystic fibrosis; CGA: chlorogenic acid; CGAS: cyclic GMP-AMP synthase; CHUK/IKKα: component of inhibitor of nuclear factor kappa B kinase complex; CLP: cecal ligation and puncture; CLR: clarithromycin; CMA: chaperone-mediated autophagy; CoV: coronavirus; DHT: dihydrotanshinone I; EGCG: epigallocatechin-3-gallate; EIF2A: eukaryotic translation initiation factor 2A; EIF2AK2: eukaryotic translation initiation factor 2 alpha kinase 2; ESKAPE: , and spp.; ESRRA: estrogen related receptor alpha; FOXO1: forkhead box O1; FUNDC1: FUN14 domain containing 1; HBV: hepatitis B virus; HCV: hepatitis C virus; HDT: host-directed therapy; HIV: human immunodeficiency virus; HMGB1: high mobility group box 1; HSV: herpes simplex virus; IAV: influenza A virus; ICT: isocryptotanshinone; IFN: interferon; IKBKB/IKKβ: inhibitor of nuclear factor kappa B kinase subunit beta; IL: interleukin; INH: isoniazid; IRF3: IFN regulatory factor 3; KEAP1: kelch like ECH associated protein 1; LAMP: lysosomal associated membrane protein; LAP: LC3-associated phagocytosis; LPS: lipopolysaccharide; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAPK: mitogen-activated protein kinase; MDM: monocyte-derived macrophage; MDR: multidrug-resistant; MON: monotropein; Mtb: ; MTOR: mechanistic target of rapamycin kinase; mtROS: mitochondrial ROS; NET: neutrophil extracellular trap; NFE2L2/Nrf2: NFE2 like bZIP transcription factor 2; NFKB/NF-κB: nuclear factor kappa B; NLRP3: NLR family pyrin domain containing 3; NLRX1: NLR family member X1; NOTCH1: notch receptor 1; NTM: nontuberculous mycobacteria; OMS: ohmyungsamycin; PAK1: p21 (RAC1) activated kinase 1; PINK1: PTEN induced kinase 1; PKM/PKM2: pyruvate kinase M1/2; PLD: phospholipase D; PM: peritoneal macrophage; PPM1A: protein phosphatase, Mg2+/Mn2+ dependent 1A; PRKN/parkin: parkin RBR E3 ubiquitin protein ligase; PtdIns3K: phosphatidylinositol 3-kinase; PtdIns3P: phosphatidylinositol-3-phosphate; PTEN: phosphatase and tensin homolog; RB1CC1/FIP200: RB1 inducible coiled-coil 1; RELA/p65: RELA proto-oncogene, NF-kB subunit; RIF: rifampicin; ROS: reactive oxygen species; RSV: resveratrol; RUBCN/rubicon: rubicon autophagy regulator; SAR: selective autophagy receptor; SIRT: sirtuin; STING1: stimulator of interferon response cGAMP interactor 1; STX17: syntaxin 17; Tat: trans-activator of transcription; TB: tuberculosis; TBK1: TANK binding kinase 1; TFEB: transcription factor EB; TLR: toll like receptor; TNA: tanshinone IIA; TNF: tumor necrosis factor; UA: ursolic acid; ULK1/Atg1: unc-51 like autophagy activating kinase 1; UPR: unfolded protein response; UVRAG: UV radiation resistance associated; VAMP8: vesicle associated membrane protein 8; VDR: vitamin D receptor; WIPI2: WD repeat domain, phosphoinositide interacting 2; ZFYVE1/DFCP1: zinc finger FYVE-type containing 1; ZIKV: Zika virus. - Source: PubMed
Publication date: 2026/04/28
Paik SeungwhaUm SoohyunKim In SooPark Eun-JinKim Kyung TaeBasu JoyotiOh Dong-ChanJo Eun-Kyeong