CHCHD3 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- CHCHD3 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00054927-T03
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CHCHD3 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: CHCHD3 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- CHCHD3 NIH gene
- Name:
- coiled-coil-helix-coiled-coil-helix domain containing 3
- Previous symbol:
- -
- Synonyms:
- FLJ20420, MINOS3, PPP1R22, Mic19, MICOS19
- Chromosome:
- 7q32.3-q33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-19
- Date modifiied:
- 2018-11-16
Related products to: CHCHD3 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: CHCHD3 293T Cell Transient Overexpression Lysate(Denatured)
- Mitochondrial bioenergetic competence critically depends on cristae architecture, which is organized and stabilized by the mitochondrial contact site and cristae organizing system (MICOS) complex. As a core MICOS subunit, CHCHD3 (also known as MIC19) contributes to assembly of the mitochondrial intermembrane space bridging (MIB) supercomplex and regulates cristae morphology, endoplasmic reticulum-mitochondria contact sites, and cellular metabolic homeostasis. Aberrant CHCHD3 expression or functional deficiency is implicated in the pathogenesis of neurodegenerative disorders, cardiovascular diseases, metabolic syndromes, and cancers. Notably, CHCHD3 function is governed by a dose-dependent "Goldilocks" principle, wherein both insufficient and excessive expression-as well as preserved abundance with impaired functional integrity-can compromise mitochondrial homeostasis, underscoring the need for context-specific therapeutic modulation. Here, we systematically summarize CHCHD3 molecular characteristics and post-translational modification networks, with emphasis on its roles in energy metabolism, organelle crosstalk, and apoptosis. We further examine the mechanistic links between CHCHD3 dysregulation and disease pathogenesis, evaluate current targeting strategies and their pharmacological limitations, and identify remaining controversies and knowledge gaps to guide future research toward clinical translation. - Source: PubMed
Publication date: 2026/06/11
Kuai Zheng TaiZheng Xiao MinLi Yue YueWang Tian Qi - Mitochondria are essential organelles for cellular metabolism and tumor formation. We discovered that CHCHD3 is an important inner mitochondria membrane protein involved in the proliferation of lung adenocarcinoma (LUAD). However, the molecular pathways through which CHCHD3 contributes to cancer progression remain poorly understood. - Source: PubMed
Publication date: 2026/06/08
Jin LiliShen JiahaoXu XutingNiu PingpingZhou YuDong ShunliShen QibinGu Qinhua - Indigenous cattle account for approximately 80% of Uganda's cattle population. These animals are well adapted to the country's ten agroecological zones and are mainly kept under pastoral and agropastoral systems. Unlike commercial breeds, they thrive on low-quality feeds, while tolerating major tropical diseases and parasites including tsetse flies, ticks, and vector-borne infections. Whole-genome sequence (WGS) analysis offers opportunities to uncover genomic regions underlying these adaptations and to trace the genetic footprints of long-term breeding decisions taken by cattle keepers. In this study, WGS data from 95 animals representing six indigenous cattle populations (Ankole, Karamojong, Nganda10, Nganda17, Nkedi, and Ntuku) were analyzed to identify genomic regions under putative selection. Two complementary approaches were applied: enumeration of the µ-statistic in RAiSD and runs of homozygosity (ROH) analysis. RAiSD identified population-level signals, while conserved ROH regions were defined using breed-specific SNP-incidence thresholds. The two methods identified 803 and 49 candidate genes respectively. The top genes identified included SLC37A1 (BTA1), CHCHD3 (BTA4), and RAB3GAP1 (BTA2) detected by RAiSD, and IL26 (BTA5), FBXL7 (BTA20), and HSPA9 (BTA7) contained in ROH. Furthermore, the regions harbored 107 novel genes (92 detected by RAiSD and 15 by ROH), corresponding to 255 quantitative trait loci. The identified genes under putative selection are associated with economically important traits including adaptation to tropical environments, resistance to parasites and diseases, and other farmer-preferred characteristics. These findings provide insights into the genetic basis of adaptation, selection and production in Ugandan indigenous cattle, supporting conservation and breeding strategies to enhance resilience and productivity. - Source: PubMed
Publication date: 2026/01/28
Okwasiimire RodneyKugonza Donald RGao JunxinWeldenegodguad MelakMakgahlela Mahlako LGhanem NasserGinja CatarinaCrooijmans Richard P M AKantanen JuhaUimari PekkaPokharel Kisun - Nuclear androgen receptor (AR) dysregulation characterizes polycystic ovary syndrome (PCOS) pathophysiology and contributes to mitochondrial dysfunction-related adverse pregnancy outcomes. However, ARs also localize to mitochondria in many cell types, and mitochondrial dysfunction is implicated in the underlying pathogenesis of PCOS. In this study, human endometrial decidual basalis tissues and rat gravid uterine tissues were collected, and subcellular fractionation, western blot, quantitative real-time polymerase chain reaction (qPCR), electron microscopy, and enzyme-linked immunosorbent assay (ELISA) were conducted. PCOS patients with early pregnancy exhibited increased expression of AR mRNA and mitochondrial AR protein in decidual basalis. Similar alterations of AR levels were also observed in gravid uterus of 5α-dihydrotestosterone (DHT) + insulin-exposed pregnant rats with fetal loss. In both PCOS patients and DHT + insulin-exposed pregnant rats, uterine mitochondria displayed disorganized cristae along with decreased uterine mitochondrial DNA (mtDNA) content and reduced expression of mitochondrial morphogenesis (mito-morphosis) genes (sorting and assembly machinery component 50 (SAMM50), coiled-coil helix coiled-coil helix domain-containing protein 3 (CHCHD3), and dynamin-related protein 1 (DRP1)) and total adenosine triphosphate (ATP) levels. In addition, there was dysregulated expression of mitochondrial fusion and fission, biogenesis, mitophagy, and mitochondrial ribosome protein gene. In DHT + insulin-exposed pregnant rats, treatment with flutamide prevented fetal loss and partially rescued mitochondrial morphological abnormalities in uterine decidual stromal cells. In addition, flutamide normalized uterine Ar mRNA and mitochondrial AR protein expression; inner membrane mitochondrial protein (Immt), ras homolog enriched in brain protein (Rheb), and Mrp7 mRNA expression; and the Parkin:PTEM-induced putative kinase 1 (Pink1) ratio and restored total nicotinamide adenine dinucleotide (NAD) and ATP contents. Collectively, this work identifies mitochondrial AR in the uterus and implicates hyperandrogenism-induced, AR-dependent mitochondrial dysfunction in decidual stromal cells as a key mechanism underlying pregnancy loss in PCOS. - Source: PubMed
Publication date: 2026/01/28
Zhang YuehuiHu MinShao Linus RLu LingjingHan JingGuo TingtingJiang MengWu YaoHan HanCui PengBrännström MatsSferruzzi-Perri Amanda NancyBillig Håkan - Thoracic SMARCA4-deficient undifferentiated tumor (SMARCA4d-UT) is an uncommon, aggressive lung neoplasm associated with smoking and characterized by loss of SMARCA4 (BRG-1) expression. Although originally considered to be a primary sarcoma, there is growing evidence that these lesions may represent transformation of conventional non-small cell carcinoma. In this study, we probe this relationship based on the clinical, histologic and molecular findings of 18 SMARCA4-deficient malignancies of the lung. Cases diagnosed as SMARCA4d-UT and SMARCA4-deficient carcinoma were retrospectively reviewed, including histologic and immunophenotypic features, and next generation sequencing studies. Of the 18 tumors, 5 were considered to represent undifferentiated SMARCA4d-UT, and 13 SMARCA4-deficient carcinomas, including 11 adenocarcinomas, 1 squamous cell carcinoma, and 1 poorly differentiated non-small cell carcinoma. All 13 carcinomas had a morphologically identifiable undifferentiated component. Survival outcomes were similar in both SMARCA4d-UT and carcinomas. Genetic alterations often seen in lung cancer were identified in 8 cases, including mutations in EGFR (in 2 SMARCA4-deficient adenocarcinomas), KRAS (1 SMARCA4d-UT and 1 SMARCA4-deficient adenocarcinoma), MAP2K1 (1 SMARCA4-deficient adenocarcinoma), and a gene fusion involving EML4::ALK (1 SMARCA4d-UT). The patient with EML4::ALK fusion was treated with alectinib with partial response. Fusions involving BRAF::CHCHD3 and FGFR1::FILIP1 were identified in 2 SMARCA4-deficient adenocarcinomas. High expression of PD-L1 (TPS >50 %) was seen in 12 cases (67 %). These finding further suggest that SMARCA4d-UT and carcinomas with SMARCA4 loss may be on the same spectrum of disease, and accurate histologic distinction between these lesions may be challenging. A unified terminology may be beneficial for appropriate diagnosis and treatment. - Source: PubMed
Publication date: 2025/12/05
D'Ambrosio DanielleFrazzette NicholasSnuderl MatijaJour George KShaffer Emily MZhou FangNarula NavneetMoreira Andre LMantilla Jose G