MAP3K5 (phospho S83) polyclonal antibody
- Known as:
- MAP3K5 (phosphorilated S83) pab (anti-)
- Catalog number:
- PAB9947
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- MAP3K5 (phospho S83) polyclonal antibody
Related genes to: MAP3K5 (phospho S83) polyclonal antibody
- Gene:
- LRRC32 NIH gene
- Name:
- leucine rich repeat containing 32
- Previous symbol:
- D11S833E, GARP
- Synonyms:
- -
- Chromosome:
- 11q13.5
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-15
- Date modifiied:
- 2016-10-05
- Gene:
- MAP3K5 NIH gene
- Name:
- mitogen-activated protein kinase kinase kinase 5
- Previous symbol:
- MEKK5
- Synonyms:
- MAPKKK5, ASK1
- Chromosome:
- 6q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-14
- Date modifiied:
- 2016-10-05
Related products to: MAP3K5 (phospho S83) polyclonal antibody
Related articles to: MAP3K5 (phospho S83) polyclonal antibody
- Due to the substantial secretory burden, bovine mammary epithelial cells (BMECs) are highly susceptible to endoplasmic reticulum (ER) stress caused by the accumulation of misfolded proteins when protein-folding capacity is overwhelmed. However, how ATF3 regulates ER stress-induced impairment of milk synthesis and apoptosis in BMECs, particularly through its direct transcriptional targets, remains poorly understood. In this study, we investigated the protective role of activating transcription factor 3 (ATF3) against ER stress-induced impairment of milk synthesis in BMECs. Using a tunicamycin-induced ER stress model, we overexpressed in BMECs and performed integrated RNA-seq and ChIP-seq analyses to elucidate the underlying molecular mechanisms. Our results indicated that ER stress disrupted milk protein and fat synthesis in BMECs by suppressing the expression of CSN2, FASN, FABP3 and promoting apoptosis via upregulation of BAX and CASP3. overexpression effectively attenuated these effects, reducing apoptosis and restoring the expression of milk fat-related genes. Transcriptomics demonstrated that ATF3 activated MAPK and PI3K-Akt signaling and lipid metabolism pathways, significantly upregulating key genes involved in fatty acid uptake, transport, and metabolism (, , , ). Integrated RNA-seq and ChIP-seq analyses identified 81 overlapping genes, with , , , and confirmed as direct transcriptional targets of ATF3, mediating its regulation of the MAPK pathway. Collectively, these findings elucidate the protective role of ATF3 against ER stress-induced lactation disruption and offer potential molecular targets for enhancing lactation resilience in dairy cattle under stress. - Source: PubMed
Publication date: 2026/05/10
Zhang ChenDai WentingLiu YueXu HongweiLiu Hongyun - Liver fibrosis (LF) is an abnormal repair reaction after chronic liver injury. Currently, adipose-derived mesenchymal stem cells (ADSCs) are widely used in the treatment of liver diseases. However, the therapeutic effect of ADSCs is affected by the damaged microenvironment. In this study, a resveratrol-functionalized nano‑selenium (Res@SeNPs) formulation was prepared to investigate whether Res@SeNPs pretreatment can enhance the therapeutic effect and alter the potential mechanism of ADSCs in carbon tetrachloride (CCl) -induced LF in mice. - Source: PubMed
Publication date: 2026/05/17
Liu ShuangjuanZhang ZiqiangLuo DongliuWen FengyunZhu XueminChen XiaoguangZhang TianaoFeng JingwenHou LeyaoLiu Yumei - There are few studies on the genomics of heat stress response and the molecular mechanisms of thermoregulation. In this experimental model, Sprague-Dawley rats were subjected to temperatures of 22 ± 1 °C (control group; CT) and 42 °C for varying durations (30, 60, and 120 min, H30, H60, and H120, respectively). Significantly high rectal body temperatures were recorded post-heat stress across all treatment groups. Adrenal corticosterone levels increased significantly, especially in H120 group. Heat stress predictive accuracies of adrenal corticosterone at H60 and H120 were higher with relatively high sensitivity and AUC greater than 0.85. RNA-sequencing of adrenal gland tissue from CT vs. H30, CT vs. H60, and CT vs. H120 identified 4, 8 and 8 known; and 72, 305 and 160 de novo differentially expressed lncRNA (DElncRNAs), respectively. A total of 61, 208, and 124 genes were found to interact with DElncRNAs in the three comparisons, of which 1, 24, and 20 were differentially expressed transcripts (DETs), respectively. Among these known DElncRNAs, Gng 2-202, MAFK-203, Rab32-201, AABR07048992.1-201 were enriched in all three comparisons. Functional enrichment and interaction network analysis of DETs interacting with DElncRNAs indicated their enrichment in pathways related to inflammation-metabolism nexus determined by DETs like Jun, Map3k5, Cyp1b1, Tiparp, Ezh2, and Cbx4. This study will supplement our understanding of the transcriptome level response mechanism of rat adrenal tissue under heat stress and provide theoretical reference for the study of mammalian body response to heat stress stimulation. - Source: PubMed
Publication date: 2026/05/16
Gu JingyiSammad AbdulGuo RenyunKang ShuaiMuniz Maria Malane MagalhãesXu YaxiSheng XihuiDou Jinhuan - Lipophagy, a selective form of macroautophagy/autophagy, degrades lipid droplets (LDs) to provide energy and is implicated in metabolic disorders. The molecular mechanism underlying lipophagy induction remains incompletely understood. This study explored the role of SETDB1 in starvation-induced autophagy and lipophagy. We demonstrate that SETDB1 deficiency exacerbates starvation-induced hepatic lipid accumulation by inhibiting lipophagy. Mechanistically, starvation promotes ATM-mediated phosphorylation of SETDB1, which enhances its interaction with and methylation of the RNA helicase DDX5. In -knockout hepatocytes, hypomethylation of DDX5 facilitates the formation of the DDX5-METTL3-METTL14 complex, increasing mA modification of and mRNAs. This modification promoted YTHDF2-mediated decay of these transcripts, thereby inhibiting starvation-induced autophagy and lipophagy. Furthermore, administration of the SETDB1 activator -59 significantly enhances lipophagy and attenuates starvation-induced hepatic steatosis. Collectively, our findings reveal a novel pathway in which SETDB1 deficiency drives mA-mediated mRNA degradation to suppress lipophagy, thereby contributing to hepatic steatosis. AA free: amino acid deprivation; ATG14: autophagy related 14; ATG5: autophagy related 5; ATG7: autophagy related 7; ATM: ATM serine/threonine kinase; Baf A1: bafilomycin A; DDX5: DEAD-box helicase 5; FASN: fatty acid synthase; LAMP1: lysosome associated membrane protein 1; LAMP2A: lysosome associated membrane protein 2A; LIPE/HSL: lipase E, hormone sensitive type; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MAP3K5/ASK1: mitogen-activated protein kinase kinase kinase 5; METTL3: methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit; METTL14: methyltransferase 14, N6-adenosine-methyltransferase non-catalytic subunit; MGLL/MGL: monoglyceride lipase; OA: oleic acid; OSBPL8/ORP8: oxysterol binding protein like 8; PLIN2: perilipin 2; PNPLA2/ATGL: patatin like domain 2, triacylglycerol lipase; SETDB1: SET domain bifurcated histone lysine methyltransferase 1; TFEB: transcription factor EB; TP53/p53: tumor protein p53; ULK1: unc-51 like autophagy activating kinase 1; YTHDF2: YTH N6-methyladenosine RNA binding protein F2. - Source: PubMed
Publication date: 2026/05/17
Wang WenjunWang YanhongHou LigeWei XiaoyunGuo WenqiHuang JuanTan JunyangLu QiuxiaZhao QiJu ZhenyuLi JianshuangZhou Qinghua - Transdifferentiation of alveolar type 2 (AT2) epithelial cells into type 1 (AT1) cells is essential for maintaining lung homeostasis and facilitating repair following injury. However, the molecular mechanisms governing AT2-to-AT1 transdifferentiation remain unclear. - Source: PubMed
Publication date: 2026/03/15
Yu TingtingLiu JiaoMa YuxinWang LuWang YuhongPan TingChen PeijieLiu QianWang Jiong-WeiChen HuaiyongWu XudongChen JunHu XuefeiTao BoShen Yujun