MYO1E Antibody (N-term) Blocking Peptide
- Known as:
- MYO1E Antibody (N-terminus) Blocking Peptide
- Catalog number:
- BP16650a
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- MYO1E Antibody (N-term) Blocking Peptide
Related genes to: MYO1E Antibody (N-term) Blocking Peptide
- Gene:
- MYO1E NIH gene
- Name:
- myosin IE
- Previous symbol:
- -
- Synonyms:
- MYO1C, HuncM-IC, MGC104638
- Chromosome:
- 15q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-04
- Date modifiied:
- 2015-07-22
Related products to: MYO1E Antibody (N-term) Blocking Peptide
Related articles to: MYO1E Antibody (N-term) Blocking Peptide
- Excessive abdominal fat deposition reduces production efficiency and metabolic health, whereas yolk lipid content is directly linked to egg quality and reproductive output. These two fat-related traits are often in conflict from a breeding perspective, yet whether they share common genetic and molecular determinants-and whether such sharing could inform divergent selection for lean abdomen with lipid‑rich yolk-remains unclear. Here, we analyzed 22 fat deposition-related traits in a population of 248 laying hens, together with genome-wide genotyping data, transcriptomic data from 10 tissues. Our results showed marked heterogeneity in the genetic architecture of fat deposition-related traits, with a higher degree of signal sharing among biologically related traits but limited overlap across different trait categories. Multi-trait association and trait-trait colocalization analyses further identified multiple shared loci between abdominal fat-related (AF) and egg yolk-related (EY) traits, including several shared candidate signals on chromosomes 2, 10, and 11. Integrative analyses incorporating multi-tissue cis-eQTL data further prioritized shared candidate regulatory genes, including MYO10, GPT2, VPS35, ADAM10, ALDH1A2, and MYO1E. Representative AF-EY shared loci, including 2__74614272, rs318039150, and rs741038415, showed opposite effect tendencies between abdominal fat- and yolk-related traits, whereas loci involving ADAM10, ALDH1A2, and MYO1E showed more directionally consistent associations, indicating both potential antagonistic and coordinated regulatory relationships. Together, these findings reveal a complex shared molecular basis linking abdominal fat deposition and yolk lipid deposition during the extended laying period and provide a framework for dissecting coordinated regulatory mechanisms and informing molecular breeding in laying hens. - Source: PubMed
Publication date: 2026/05/27
Zhang WenxinLan FangrenCai RonglangYang NingSun Congjiao - Phagocytosis requires coordinated remodeling of the actin cytoskeleton to generate protrusive and contractile forces that drive target engulfment. Class I myosins Myo1e and Myo1f (Myo1e/f) have been implicated in linking the plasma membrane to the actin network, but their specific roles during Fc-receptor-mediated phagocytosis remain unclear. Using CRISPR-edited RAW 264.7 macrophages lacking Myo1e and Myo1f, we show that double knockout (dKO) cells exhibit markedly reduced uptake of IgG-coated beads, a phenotype that is partially rescued by re-expression of either myosin. Lattice-light-sheet and confocal imaging revealed distinct F-actin architectures corresponding to the various stages of cup progression, including basal podosome-like adhesions, individual phagocytic podosomes (actin teeth) along the rim of the cup, and a contractile phagocytic ring formed by the reorganization of podosomes into a higher-order network. In Myo1e/f-deficient cells, podosome formation was diminished, actin teeth were largely absent, and the phagocytic ring formed prematurely, which was often accompanied by stalled cup progression and repeated engulfment attempts. Myo1e/f localized both to podosomes and to the inner surface of the phagocytic ring, non-muscle myosin II (NM2) localized to the outer surface, and the absence of Myo1e/f correlated with the diffuse distribution of NM2. In addition, Myo1e/f-deficient macrophages exhibited increased trogocytosis of antibody-opsonized HL-60 cells, indicating a shift from whole-target engulfment toward partial target ingestion. These results suggest that Myo1e/f coordinate spatial and temporal transitions between protrusive and contractile actin networks, thereby ensuring efficient phagocytic cup progression. Our findings highlight a dual role for Myo1e/f in adhesion regulation and force balance during macrophage phagocytosis. - Source: PubMed
Publication date: 2026/05/01
Paul T CLoyd Y MChase S EO'Connor T WHobson C MLee R MVorselen DKrendel M - - Source: PubMed
Publication date: 2026/04/13
Xu MengqiOstap E Michael - Cholesterol must be precisely partitioned within cells, with the plasma membrane (PM) holding the highest levels. In contrast, the endoplasmic reticulum (ER)-the site of cholesterol synthesis-contains very little cholesterol. How newly synthesized cholesterol moves from the ER to the PM remains poorly defined. Here, we identify a COPII-independent trafficking route in which nascent cholesterol is exported via specialized cholesterol transport vesicles (CTVs). A genome-wide screen reveals that DEGS1-derived ceramide is essential for CTV formation at the ER. Biochemical purification shows that caveolins serve as the vesicle coat, and loss of caveolins eliminates CTV production. Silencing PACSINs or dynamins leads to intracellular accumulation of CTVs, suggesting impaired vesicle scission. CTV delivery to the PM depends on actin filaments and the motors MYO1C and MYO1E. In vitro reconstitution with giant unilamellar vesicles demonstrates that ceramide promotes inward budding, whereas CAV1 drives outward budding. This work identifies a previously unrecognized class of ER-derived, caveolin-coated vesicles that transport cholesterol to the PM. - Source: PubMed
Publication date: 2026/04/13
Sun MingLiu Yuan-BinSun Pu-YuSheng Zhao-ChenLiu Jia-WenYuan Pei-XinZhu Wen-ZhuoDeng GangWen Xing-YanZhao XiaoluLuo JieSong Bao-Liang - Temporal lobe epilepsy (TLE) remains a major clinical challenge, with over one-third of patients resistant to existing medications. Microglia, the brain's resident immune cells, are highly plastic, yet their potential to adopt a protective state in epilepsy is unclear. Using time-resolved single-nucleus RNA sequencing (snRNA-seq) in a kainic acid (KA)-induced seizure model, we identified an early-emerging microglial subpopulation transcriptionally distinct from homeostatic microglia. This subpopulation was characterized by high expression of insulin-like growth factor 1 (Igf1), along with Myo1e and Apbb2. Through in vitro co-culture assays, we demonstrated that TGFB1 stimulation, but not LPS, drives the generation of this IGF1 phenotype. These induced IGF1 microglia significantly suppressed the secretion of pro-inflammatory cytokines under inflammatory conditions. Importantly, conditioned medium from IGF1 microglia enhanced the proliferation and survival of KA-exposed HT22 neuronal-like cells. Mechanistically, we found that TGFB1 activates the Wnt/β-catenin pathway, promoting the nuclear translocation of β-catenin, which in turn upregulates IGF1 expression. In vitro, we abolished the TGFB1-induced neuroprotective phenotype by knocking down β-catenin using siRNA; however, exogenous supplementation with IGF1 partially rescued this effect. Our findings define a TGFB1-β-catenin-IGF1 axis that drives microglia into a neuroprotective state, revealing a novel endogenous mechanism and therapeutic direction for epilepsy. - Source: PubMed
Publication date: 2026/03/29
Yuan ZiweiLiu YanDuan RanZhang XiaogangHu LiqinSong FeiLiu JingMeng YuanKe PingyangXiao Fei