Polyclonal Rabbit BORG1 Antibody
- Known as:
- Polyclonal Rabbit BORG1 Antibody
- Catalog number:
- KA0427
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit BORG1 Antibody
Related genes to: Polyclonal Rabbit BORG1 Antibody
- Gene:
- CDC42EP2 NIH gene
- Name:
- CDC42 effector protein 2
- Previous symbol:
- -
- Synonyms:
- CEP2, BORG1
- Chromosome:
- 11q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-27
- Date modifiied:
- 2016-10-05
Related products to: Polyclonal Rabbit BORG1 Antibody
Related articles to: Polyclonal Rabbit BORG1 Antibody
- The regular structure of CNS myelin requires specialized structural proteins, including septin filaments composed of subunits SEPTIN2, SEPTIN4, SEPTIN7, and SEPTIN8. These filaments scaffold the innermost non-compacted myelin layer; their disruption causes pathological myelin outfoldings. However, the mechanisms that control myelin septin assembly are incompletely understood. We found that loss of CDC42 from oligodendrocytes of adult mice causes myelin pathology including outfoldings, coinciding with depletion of myelin septins and CDC42-effector proteins (CDC42EP1 and CDC42EP2). We thus tested the functional relevance of the latter by deleting both the Cdc42ep1 and Cdc42ep2-genes in oligodendrocytes. We observed myelin outfoldings as a very specific pathology, markedly reduced abundance of myelin septins, and disorganized septin filaments in myelin. Immunohistochemical analysis did not uncover astrocyte or microglial activation, implying that myelin outfoldings per se do not induce secondary neuropathology. Together, our data reveal a critical function for CDC42 and CDC42EP1/CDC42EP2 in regulating myelin septin filaments, which facilitate structural integrity of myelin sheaths. - Source: PubMed
Hümmert Sophiede Faria Joana PaesJahn OlafBilgin EgeŁukasik NikolaRao ChethanaMitkovski MišoBenseler FritzBrose NilsSiems Sophie BGoebbels SandraMöbius WiebkeEwers HelgeRelvas João BWerner Hauke B - Although studies have shown that patients with rheumatoid arthritis (RA) are at a higher risk of developing myasthenia gravis (MG), the causal relationship and shared genetic basis between these two diseases have not been fully investigated. The purpose of this study is to uncover the potential bidirectional causality between RA and MG, and to explore their shared genetic factors and possible pathogenic mechanisms. - Source: PubMed
Publication date: 2025/07/19
Huang JianWang LuHu XiaodongWang TianruiZhang Yingze - α-Synuclein (α-syn) protein is a major pathological agent of familial Parkinson's disease (PD), and its levels and aggregations determine neurotoxicity in PD pathogenesis. Although the pathophysiological functions of α-syn have been extensively studied, its biological functions remain elusive, and there are reports of wild-type (WT) α-syn and two missense mutations of α-syn (A30P and A53T) inducing protective neuritogenesis through neurite outgrowth. However, the function of another α-syn mutation, E46K, has not been fully elucidated. Thus, we compared the effect of E46K α-syn with other types to identify the mechanisms underlying neurite outgrowth. - Source: PubMed
Publication date: 2024/12/25
Jung HyunjaKim Seonghan - Superoxide Dismutase 3 (SOD3) scavenges extracellular superoxide giving a hydrogen peroxide metabolite. Both Reactive Oxygen Species diffuse through aquaporins causing oxidative stress and biomolecular damage. SOD3 is differentially expressed in cancer and this research utilises Gene Expression Omnibus data series GSE2109 with 2,158 cancer samples. Genome-wide expression correlation analysis was conducted with SOD3 as the seed gene. Categorical SOD3 Pearson Correlation gene lists incrementing in correlation strength by 0.01 from ρ≥|0.34| to ρ≥|0.41| were extracted from the data. Positively and negatively SOD3 correlated genes were separated for each list and checked for significance against disease overlapping genes in the ClinVar and Orphanet databases via Enrichr. Disease causal genes were added to the relevant gene list and checked against Gene Ontology, Phenotype Ontology, and Elsevier Pathways via Enrichr before the significant ontologies containing causal and non-overlapping genes were reviewed with a literature search for possible disease and oxidative stress associations. 12 significant individually discriminated disorders were identified: Autosomal Dominant Cutis Laxa (p = 6.05x10-7), Renal Tubular Dysgenesis of Genetic Origin (p = 6.05x10-7), Lethal Arteriopathy Syndrome due to Fibulin-4 Deficiency (p = 6.54x10-9), EMILIN-1-related Connective Tissue Disease (p = 6.54x10-9), Holt-Oram Syndrome (p = 7.72x10-10), Multisystemic Smooth Muscle Dysfunction Syndrome (p = 9.95x10-15), Distal Hereditary Motor Neuropathy type 2 (p = 4.48x10-7), Congenital Glaucoma (p = 5.24x210-9), Megacystis-Microcolon-Intestinal Hypoperistalsis Syndrome (p = 3.77x10-16), Classical-like Ehlers-Danlos Syndrome type 1 (p = 3.77x10-16), Retinoblastoma (p = 1.9x10-8), and Lynch Syndrome (p = 5.04x10-9). 35 novel (21 unique) genes across 12 disorders were identified: ADNP, AOC3, CDC42EP2, CHTOP, CNN1, DES, FOXF1, FXR1, HLTF, KCNMB1, MTF2, MYH11, PLN, PNPLA2, REST, SGCA, SORBS1, SYNPO2, TAGLN, WAPL, and ZMYM4. These genes are proffered as potential biomarkers or therapeutic targets for the corresponding rare diseases discussed. - Source: PubMed
Publication date: 2024/10/31
Stanworth MarkZhang Shu-Dong - Bone marrow failure (BMF) is chronic benzene-induced hematotoxicity, which is associated with differential gene expression abnormality. Benzene-induced BMF is characterized by irreversible bone marrow depression. Despite extensive studies have been conducted, there is a lack of reliable, useful and simple diagnostic method for BMF. Previous studies have shown that the aberrant gene expression changes and reactive oxygen species production in bone marrow cells related to the development of BMF. Early detection of differentially expressed genes (DEGs) as potential biomarkers is important for diagnosis and treatment. However, the validation of effective biomarker through DEGs analysis in benzene-induced BMF still deserve to be clarified. This study aimed to identify target genes as potential biomarkers with benzene-induced BMF based on DEGs analysis. - Source: PubMed
Publication date: 2024/08/03
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