Tumor Necrosis Factor Alpha (TNF-α), Monoclonal Antibodies to Human Cytokines and Growth Factors, Host:Mouse, Isotype: IgG1,k, Clone: CH8810, Aff. pur.
- Known as:
- Tumor Necrosis Factor Alpha (TNF-α), Monoclonal Antibodies Human Cytokines Growth Factors, Host:Mouse, Isotype: IgG1,k, Clone: CH8810, Aff. pur.
- Catalog number:
- MO-C40003A
- Product Quantity:
- 0.5 mg
- Category:
- -
- Supplier:
- Anogen
- Gene target:
- Tumor Necrosis Factor Alpha (TNF-α) Monoclonal Antibodies Human Cytokines and Growth Factors Host:Mouse Isotype: IgG1 Clone: CH8810 Aff. pur.
Related genes to: Tumor Necrosis Factor Alpha (TNF-α), Monoclonal Antibodies to Human Cytokines and Growth Factors, Host:Mouse, Isotype: IgG1,k, Clone: CH8810, Aff. pur.
- Gene:
- BTF3P11 NIH gene
- Name:
- basic transcription factor 3 pseudogene 11
- Previous symbol:
- BTF3L1
- Synonyms:
- HUMBTFB, TNFRSF11B, OPG, OCIF
- Chromosome:
- 13q22.3
- Locus Type:
- pseudogene
- Date approved:
- 1997-12-12
- Date modifiied:
- 2016-10-05
- Gene:
- C1QL1 NIH gene
- Name:
- complement C1q like 1
- Previous symbol:
- -
- Synonyms:
- CRF, C1QRF, C1QTNF14, CTRP14
- Chromosome:
- 17q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-06
- Date modifiied:
- 2018-07-16
- Gene:
- C1QL2 NIH gene
- Name:
- complement C1q like 2
- Previous symbol:
- -
- Synonyms:
- CTRP10, C1QTNF10
- Chromosome:
- 2q14.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-18
- Date modifiied:
- 2016-07-04
- Gene:
- C1QL3 NIH gene
- Name:
- complement C1q like 3
- Previous symbol:
- -
- Synonyms:
- K100, C1ql, C1QTNF13, CTRP13
- Chromosome:
- 10p13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-19
- Date modifiied:
- 2018-11-15
- Gene:
- C1QL4 NIH gene
- Name:
- complement C1q like 4
- Previous symbol:
- -
- Synonyms:
- C1QTNF11, CTRP11
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-22
- Date modifiied:
- 2016-07-04
Related products to: Tumor Necrosis Factor Alpha (TNF-α), Monoclonal Antibodies to Human Cytokines and Growth Factors, Host:Mouse, Isotype: IgG1,k, Clone: CH8810, Aff. pur.
Related articles to: Tumor Necrosis Factor Alpha (TNF-α), Monoclonal Antibodies to Human Cytokines and Growth Factors, Host:Mouse, Isotype: IgG1,k, Clone: CH8810, Aff. pur.
- This paper is part of a series of publications developed by the Latin America-Comet assay (LA-COMET) group, which emerged in 2021, during the Asociacion Latinoamericana de Mutagenesis, Carcinogenesis y Teratogenesis Ambiental Congress, to organize the LA-COMET initiative. A total of 104 alkaline comet assay publications in animal (aquatic and terrestrial) and plant models, authored by members of this group, were analyzed to determine how DNA damage under experimental and environmental exposure conditions is assessed. The manuscript reflects the broad use and versatility of the comet assay in diverse taxonomic groups (invertebrates and vertebrates), in vivo research models, and cell types (e.g., erythrocytes, branchia cells, retinal epithelial cells, peripheral blood, liver, kidney, lung, bone marrow, testicle and nasal cells). Application of the comet assay in diverse biological systems requires careful methodological standardization to ensure reproducibility and allow for comparability of results. In order to unify the evaluations of the papers, a quality score system was developed, the 'quality score comet assay' (QSca), providing values reflecting the methodological rigor of the execution of the assay. The group identified key elements when performing the comet assay and uses them as the focus for the QSca score. The LA-COMET initiative will provide opportunities to strengthen collaborative networks among Latin American countries, promoting more integrative and regionally connected research where the comet assay can be used as a reliable and reproducible tool for the assessment of DNA damage in diverse biological models. - Source: PubMed
Publication date: 2026/05/21
Poletta Gisela LMussali-Galante PatriciaCastillo-Ipiña J AlfredoEspinosa-Reyes GuillermoFlores-Márquez Ana RosaGonzález-Mille Donaji JIlizaliturri-Hernández César ARuiz de Arcaute CelesteTovar-Sánchez Efraínda Silva JulianaFranco DeidamiaGarcía Ana LeticiaLafon-Hughes LauraLeón-Mejía GrethelNarváez Diana MPacheco-Pantoja Elda LeonorRojas EmilioSimoniello María FernandaSoloneski SoniaTirado NoemiYáñez-Estrada LeticiaValverde MaharaGómez-Arroyo Sandra - The SPINK2 protein, encoded by the SPINK2 gene, plays an essential role in the normal development of spermatozoa, and its deficiency is associated with spermatogenesis disorders ranging from aspermia to azoospermia. This study aimed to identify the most deleterious variants of the SPINK2 gene and to evaluate their effects on protein structure and function through an in silico approach. A total of 8,028 variants were identified, including 72 missense variants. Using 11 bioinformatics tools, six variants (P50L, T58I, C66Y, E62A, P42S, and P45L) were predicted to have deleterious effects. Protein-protein interaction analysis using the STRING database revealed strong functional associations between SPINK2, SPINK1, and ACR, and medium-confidence associations with SPINK4, SPINK13, PMPCA, KLK4, SPINK9, SPINK6, SPACA1, and NUDT8. Local structural analysis showed that variants such as T58I and C66Y gained additional hydrophobic interactions, whereas P50L and P42S lost key interactions, potentially impairing protein stability and function. Molecular dynamics simulations using GROMACS revealed that P50L enhances protein stability, reduces amino acid flexibility, and increases the overall dimensions of the protein. T58I had a mild effect on stability, whereas E62A and C66Y decreased stability and flexibility while increasing protein size. P42S and P45L induced slight stability alterations, reduced flexibility, and enlarged the protein. Overall, these structural and dynamic changes suggest functional impairment of SPINK2. To our knowledge, this is the first study to identify six deleterious SPINK2 variants with potential roles in the disruption of spermatogenesis, providing a foundation for future functional and clinical investigations. - Source: PubMed
Publication date: 2026/01/30
Elkarhat GhitaAit Benichou SamahRedouane SalaheddineBarakat AbdelhamidSoukri AbdelazizEl Khalfi BouchraRouba Hassan - Diabetic peripheral neuropathy (DPN), the most prevalent complication of diabetes, currently lacks disease-modifying therapies. While Tangluoning recipe (TLN)-a traditional Chinese herbal medicine derived from Huangqi Guizhi Wuwu decoction-demonstrates therapeutic efficacy against DPN symptoms, its mechanism remained elusive. This study pioneers two transformative advances: Uncovering a previously unrecognized pathogenic axis linking mitochondrial thioredoxin (Trx2) deficiency to DPN demyelination; Establishing a novel dual-target therapeutic strategy that concurrently rescues mitochondrial dysfunction and lipid metabolic homeostasis. - Source: PubMed
Publication date: 2025/12/03
Zhu YanboLi XiaoGao YingyingTie YanLiu HaolongYang XinweiXu Liping - This study intended to explore the molecular mechanisms and the mitochondrial metabolic characteristics of sepsis-associated acute kidney injury (S-AKI) through bioinformatics analysis and experimental validation. - Source: PubMed
Publication date: 2025/10/17
Xia YichunQian YimingHu GuanyuPu YuehongGuo Jian - Autosomal recessive cerebellar ataxias (ARCA) are rare heterogenous neurodegenerative disorders characterized by degeneration of the cerebellum and spinal cord with an early onset before the age of 20 years. PMPCA (MIM: 613036), is a key enzyme in mitochondrial protein processing which is critical for cell survival and growth. Our objective was to investigate Peptidase, Mitochondrial Processing Subunit Alpha (PMPCA) mutations linked with Spinocerebellar ataxia, autosomal recessive 2 (SCAR2). - Source: PubMed
Bagabir Hala AbubakerAbdulkareem Angham AbdulrhmanMuthaffar Osama YousefShirah Bader HNaseer Muhammad Imran