MYPOP antibody - N-terminal region (P100709_P050)
- Known as:
- MYPOP (anti-) - N-terminal region (P100709_P050)
- Catalog number:
- p100709_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MYPOP antibody - N-terminal region (P100709_P050)
Related genes to: MYPOP antibody - N-terminal region (P100709_P050)
- Gene:
- MYPOP NIH gene
- Name:
- Myb related transcription factor, partner of profilin
- Previous symbol:
- -
- Synonyms:
- P42pop
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 2009-02-23
- Date modifiied:
- 2016-06-22
Related products to: MYPOP antibody - N-terminal region (P100709_P050)
Related articles to: MYPOP antibody - N-terminal region (P100709_P050)
- Insulin resistance is the decreased effectiveness of insulin receptor function during signaling of glucose uptake. Insulin receptors are regulated by endocytosis, a process that removes receptors from the cell surface to be marked for degradation or for re-use. - Source: PubMed
Publication date: 2023/09/27
Tim BryceKouznetsova Valentina LKesari SantoshTsigelny Igor F - Current studies on actin function primarily rely on cytoplasmic actin due to the absence of cellular models specifically expressing nuclear actin. Here, cell models capable of expressing varying levels of nuclear F/G-actin are generated and a significant role of nuclear actin in the regulation of epithelial-mesenchymal transition (EMT) is uncovered. Through immunoprecipitation and mass spectrometry analyses, distinct binding partners for nuclear F-actin (β-catenin, SMAD2, and SMAD3) and nuclear G-actin (MYBBP1A, NKRF, and MYPOP) are investigated, which respectively modulate EMT-promoting and EMT-repressing transcriptional events. While nuclear F-actin promotes EMT with enhanced cell migration, survival, and elongated mesenchymal morphology, nuclear G-actin represses EMT and related cell activities. Mechanistically, nuclear F-actin enhances β-catenin, SMAD2, and SMAD3 expression and stability in the nuclei, while nuclear G-actin increases MYBBP1A, NKRF, and MYPOP expression and stability in the nuclei. The association between nuclear F/G-actin and N-cadherin/E-cadherin in the cell lines (in vitro), and increased nuclear actin polymerization in the wound healing cells (in vivo) affirm a significant role of nuclear actin in EMT regulation. With evidence of nuclear actin polymerization and EMT during development, and irregularities in disease states such as cancer and fibrosis, targeting nuclear actin dynamics to trigger dysregulated EMT warrants ongoing study. - Source: PubMed
Publication date: 2023/08/11
Du William WQadir JaveriaDu Kevin YChen YuWu NanYang Burton B - The relationship between epilepsy and glioma has long been widely recognized, but the mechanisms of interaction remain unclear. This study aimed to investigate the shared genetic signature and treatment strategies between epilepsy and glioma. - Source: PubMed
Publication date: 2023/05/14
Zhao KaiBai XuexueWang XiaoCao YiyaoZhang LiuLi WeiWang Shiyong - The skin represents a physical and chemical barrier against invading pathogens, which is additionally supported by restriction factors that provide intrinsic cellular immunity. These factors detect viruses to block their replication cycle. Here, we uncover the Myb-related transcription factor, partner of profilin (MYPOP) as a novel antiviral protein. It is highly expressed in the epithelium and binds to the minor capsid protein L2 and the DNA of human papillomaviruses (HPV), which are the primary causative agents of cervical cancer and other tumors. The early promoter activity and early gene expression of the oncogenic HPV types 16 and 18 is potently silenced by MYPOP. Cellular MYPOP-depletion relieves the restriction of HPV16 infection, demonstrating that MYPOP acts as a restriction factor. Interestingly, we found that MYPOP protein levels are significantly reduced in diverse HPV-transformed cell lines and in HPV-induced cervical cancer. Decades ago it became clear that the early oncoproteins E6 and E7 cooperate to immortalize keratinocytes by promoting degradation of tumor suppressor proteins. Our findings suggest that E7 stimulates MYPOP degradation. Moreover, overexpression of MYPOP blocks colony formation of HPV and non-virally transformed keratinocytes, suggesting that MYPOP exhibits tumor suppressor properties. - Source: PubMed
Publication date: 2018/07/17
Wüstenhagen ElenaBoukhallouk FatimaNegwer InkaRajalingam KrishnarajStubenrauch FrankFlorin Luise - Individuals with inclusion body myopathy type 3 (IBM3) display congenital joint contractures with early-onset muscle weakness that becomes more severe in adulthood. The disease arises from an autosomal dominant point mutation causing an E706K substitution in myosin heavy chain type IIa. We have previously expressed the corresponding myosin mutation (E701K) in homozygous indirect flight muscles and recapitulated the myofibrillar degeneration and inclusion bodies observed in the human disease. We have also found that purified E701K myosin has dramatically reduced actin-sliding velocity and ATPase levels. Since IBM3 is a dominant condition, we now examine the disease state in heterozygote in order to gain a mechanistic understanding of E701K pathogenicity. Myosin ATPase activities in heterozygotes suggest that approximately equimolar levels of myosin accumulate from each allele. actin sliding velocity rates for myosin isolated from the heterozygotes were lower than the control, but higher than for the pure mutant isoform. Although sarcomeric ultrastructure was nearly wild type in young adults, mechanical analysis of skinned indirect flight muscle fibers revealed a 59% decrease in maximum oscillatory power generation and an approximately 20% reduction in the frequency at which maximum power was produced. Rate constant analyses suggest a decrease in the rate of myosin attachment to actin, with myosin spending decreased time in the strongly bound state. These mechanical alterations result in a one-third decrease in wing beat frequency and marginal flight ability. With aging, muscle ultrastructure and function progressively declined. Aged myofibrils showed Z-line streaming, consistent with the human heterozygote phenotype. Based upon the mechanical studies, we hypothesize that the mutation decreases the probability of the power stroke occurring and/or alters the degree of movement of the myosin lever arm, resulting in decreased motility, reduced muscle power output and focal myofibrillar disorganization similar to that seen in individuals with IBM3. - Source: PubMed
Publication date: 2017/03/03
Suggs Jennifer AMelkani Girish CGlasheen Bernadette MDetor Mia MMelkani AnjuMarsan Nathan PSwank Douglas MBernstein Sanford I