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Results in Journal Molecular and Cellular Biology: 31,610

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Beatriz Romartinez-Alonso, Maura Agostini, Heulyn Jones, Jayde McLellan, Deepali Sood, Nicholas Tomkinson, Federica Marelli, Ilaria Gentile, W. Edward Visser, Erik Schoenmakers, et al.
Molecular and Cellular Biology; https://doi.org/10.1128/mcb.00363-21

Abstract:
Mutations in thyroid hormone receptor α (TRα), a ligand-inducible transcription factor, cause Resistance to Thyroid Hormone α (RTHα). This disorder is characterised by tissue-specific hormone refractoriness and hypothyroidism, due to inhibition of target gene expression by mutant TRα-corepressor complexes. Using biophysical approaches, we show that RTHα-associated TRα mutants devoid of ligand-dependent transcription activation function, unexpectedly retain the ability to bind thyroid hormone. Visualisation of ligand (T3) within the crystal structure of a prototypic TRα mutant, validates this notion. This finding prompted synthesis of different thyroid hormone analogues, identifying a lead compound (ES08) which dissociates corepressor from mutant human TRα more efficaciously than T3. ES08 rescues developmental anomalies in a zebrafish model of RTHα and induces target gene expression in TRα mutation-containing cells from an RTHα patient, more effectively than T3. Our observations provide proof-of-principle for developing synthetic ligands that can relieve transcriptional repression by the mutant TRα-corepressor complex, for treatment of RTHα.
Xin Tang, Cheng Chang, Daniel Mosallaei, David T. Woodley, Axel H. Schönthal, Mei Chen, Wei Li
Molecular and Cellular Biology; https://doi.org/10.1128/mcb.00459-21

Abstract:
The rare capacity for heat shock protein-90 (Hsp90) chaperones to support almost the entire cellular signaling networks was viewed as a potential breakthrough point to combat tumor resistance to single oncogene-based therapeutics. Over two decades, several generations of Hsp90 ATP-binding inhibitors have entered numerous cancer clinical trials, but few have advanced to FDA approval for treatment of human cancers. Herein, we report that Hsp90 expression dramatically vary especially among different types of non-cancer cells and organs. The highly variable levels of Hsp90 from as low as 1.7% to as high as 9% of their total cellular proteins were responsible for either an extreme sensitivity or an extreme resistance to a classical Hsp90 ATP-binding inhibitor. Among randomly selected cancer cell lines, the same client proteins for regulation of cell growth exhibited unexpectedly heterogenous reactions in response to Hsp90 ATP-binding inhibitor, inconsistent with the current understanding. Finally, a minimum amount (<10%) of Hsp90β was still required for client protein stability and cell survival even in the presence of full Hsp90α. These new findings of Hsp90 expression in host and isoform compensation in tumor cells could complicate biomarker selection, toxicity readout and clinical efficacy of Hsp90-ATP-binding inhibitors in cancer clinical trials.
Emily Tsutsumi, Jeremiah Stricklin, Emily A. Peterson, Joyce A. Schroeder,
Molecular and Cellular Biology; https://doi.org/10.1128/mcb.00382-21

Abstract:
The chemokine Cxcl10 has been associated with poor prognosis in breast cancer, but the mechanism is not well understood. Our previous study have shown that CXCL10 was repressed by the ING4 tumor suppressor, suggesting a potential inverse functional relationship. We thus investigated a role for Cxcl10 in the context of ING4 deficiencies in breast cancer. We first analyzed public gene expression datasets and found that patients with CXCL10 -high/ ING4 -low expressing tumors had significantly reduced disease-free survival in breast cancer. In vitro , Cxcl10 induced migration of ING4 -deleted breast cancer cells, but not of ING4 -intact cells. Using inhibitors, we found that Cxcl10-induced migration of ING4 -deleted cells required Cxcr3, Egfr, and the Gβγ subunits downstream of Cxcr3, but not Gαi. Immunofluorescent imaging showed that Cxcl10 induced early transient colocalization between Cxcr3 and Egfr in both ING4 -intact and ING4 -deleted cells, which recurred only in ING4 -deleted cells. A peptide agent that binds to the internal juxtamembrane domain of Egfr inhibited Cxcr3/Egfr colocalization and cell migration. Taken together, these results presented a novel mechanism of Cxcl10 that elicits migration of ING4 -deleted cells, in part by inducing a physical or proximal association between Cxcr3 and Egfr and signaling downstream via Gβγ. These results further indicated that ING4 plays a critical role in the regulation of Cxcl10 signaling that enables breast cancer progression.
, Qian Chai, Ziying Zhang
Molecular and Cellular Biology; https://doi.org/10.1128/mcb.00282-21

Abstract:
Glycemic variability has been considered as one of the predictors of diabetes complications in patients with diabetes mellitus (DM). In this work, we evaluated whether glycemic variability induces cardiac fibrosis through regulating cardiac fibroblast activation and macrophage polarization. Moreover, we determined whether glucose transporter sodium-glucose cotransporter 1 (SGLT1) plays an important role in this process. Glycemic variability-induced mice were established using DM mice (GVDM mice) and intermittent high glucose (IHG) treatment was used to simulate glycemic variability in RAW264.7 macrophages and cardiac fibroblasts. The short hairpin RNA for SGLT1 was used to knock down SGLT1. The results showed that glycemic variability aggravated the cardiac fibrosis in GVDM mice. Additionally, glycemic variability promoted the expressions of fibrogenic cytokine and the extracellular matrix proteins in left ventricular tissues and cardiac fibroblasts. GVDM mice showed a higher incidence of macrophage infiltration and M1 polarization in left ventricular tissues. Moreover, IHG promoted RAW264.7 macrophages tended to differentiate to M1 phenotype. SGLT1 knockdown alleviated cardiac fibrosis in GVDM mice and inhibited activations of cardiac fibroblasts and macrophages M1 polarization. Our results indicated that glycemic variability aggravates cardiac fibrosis through activating cardiac fibroblast and macrophage M1 polarization, which could be partially inhibited by SGLT1 knockdown.
Sanchita Rauth, Saswati Karmakar, Ashu Shah, Parthasarathy Seshacharyulu, Rama Krishna Nimmakayala, Koelina Ganguly, Rakesh Bhatia, Sakthivel Muniyan, Sushil Kumar, Samikshan Dutta, et al.
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00135-21

Abstract:
RNA polymerase II-associated factor 1 (PAF1)/pancreatic differentiation 2 (PD2) is a core subunit of the human PAF1 complex (PAF1C) that regulates the RNA polymerase II function during transcriptional elongation. PAF1/PD2 has also been linked to the oncogenesis of pancreatic ductal adenocarcinoma (PDAC).
Rui Liu, Ashleigh King, David Tarlinton,
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00251-21

Abstract:
Toll-like receptors (TLRs) and interleukin-1 (IL-1) receptors regulate immune and inflammatory responses by activating the NF-κB pathway. Here, we report that B-cell–specific loss of Dynein light chain-1 (DYNLL1, LC8) or its designated transcription factor ASCIZ (ATMIN) leads to severely reduced in vivo antibody responses to TLR4-dependent but not T-cell–dependent antigens in mice.
Salar Ahmad, Valérie Côté,
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00056-21

Abstract:
The repair of DNA double-strand breaks (DSBs) occurs in chromatin, and several histone posttranslational modifications have been implicated in the process. Modifications of the histone H2A N-terminal tail have also been linked to DNA damage response, through acetylation or ubiquitination of lysine residues that regulate repair pathway choice.
Dheerendra Pratap Mall, Subham Basu, Koushik Ghosh, Nidhi Kumari, Abhishake Lahiri, Sandip Paul, Debabrata Biswas
Molecular and Cellular Biology; https://doi.org/10.1128/mcb.00344-21

Abstract:
Although large number of recent studies indicate strong association of FKBP5 (aka FKBP51) functions with various stress-related psychiatric disorder, the overall mechanisms are poorly understood. Beyond a few studies indicating its functions in regulating glucocorticoid receptor-, and AKT-signalling pathways, other functional roles (if any) are unclear. In this study, we report an anti-proliferative role of human FKBP5 through negative regulation of expression of proliferation-related genes. Mechanistically, we show that, owing to same region of interaction on CDK9, human FKBP5 directly competes with CyclinT1 for functional P-TEFb complex formation. In vitro biochemical coupled with cell-based assays, showed strong negative effect of FKBP5 on P-TEFb-mediated phosphorylation of diverse substrates. Consistently, FKBP5 knockdown showed enhanced P-TEFb complex formation leading to increased global RNA polymerase II CTD phosphorylation and expression of proliferation-related genes and subsequent proliferation. Thus, our results show an important role of FKBP5 in negative regulation of P-TEFb functions within mammalian cells.
Yin Duan, Hui-Ling Chen, Shuo Zhang, Fei-Xia Ma, Hong-Chen Zhang, Xiao-Ai Lv
Molecular and Cellular Biology; https://doi.org/10.1128/mcb.00163-21

Abstract:
EF24, a curcumin analog, exerts a potent anti-tumor effect on various cancers. However, whether EF24 retards the progression of triple-negative breast cancer (TNBC) remains unclear. In this study, we explored the role of EF24 in TNBC and clarified the underlying mechanism. In a mouse model of TNBC xenograft, EF24 administration reduced the tumor volume, suppressed cell proliferation, promoted cell apoptosis, and downregulated long non-coding RNA human leukocyte antigen complex group 11 (HCG11) expression. In TNBC cell lines, EF24 administration reduced cell viability, suppressed cell invasion, and downregulated HCG11 expression. HCG11 overexpression re-enhanced the proliferation and invasion of TNBC cell lines suppressed by EF24. The following mechanism research revealed that HCG11 overexpression elevated Sp1 transcription factor (Sp1) expression by reducing its ubiquitination, thereby enhanced Sp1-mediated cell survival and invasion in the TNBC cell line. Finally, the in vivo study showed that HCG11-overexpressed TNBC xenografts exhibited lower responsiveness in response to EF24 treatment. In conclusion, EF24 treatment reduced HCG11 expression, resulting in the degradation of Sp1 expression, thereby inhibiting the proliferation and invasion of TNBC cells.
Atanu Mondal, Apoorva Bhattacharya, Vipin Singh, Shruti Pandita, Albino Bacolla, Raj K. Pandita, John A. Tainer, Kenneth S. Ramos, Tej K. Pandita, Chandrima Das
Molecular and Cellular Biology; https://doi.org/10.1128/mcb.00483-21

Abstract:
From initiation through progression, cancer cells are subjected to a magnitude of endogenous and exogenous stresses, which aid in their neoplastic transformation. Exposure to these classes of stress induces imbalance in cellular homeostasis and, in response, cancer cells employ informative adaptive mechanisms to rebalance biochemical processes that facilitate survival and maintain their existence. Different kinds of stress stimuli trigger epigenetic alterations in cancer cells, which leads to changes in their transcriptome and metabolome, ultimately resulting in suppression of growth inhibition or induction of apoptosis. Whether cancer cells show a protective response to stress or succumb to cell death depends on the type of stress and duration of exposure. A thorough understanding of epigenetic and molecular architecture of cancer cell stress response pathways can unveil a plethora of information required to develop novel anti-cancer therapeutics. The present view highlights current knowledge about alterations in epigenome and transcriptome of cancer cells as a consequence of exposure to different physicochemical stressful stimuli such as reactive oxygen species (ROS), hypoxia, radiation, hyperthermia, genotoxic agents, and nutrient deprivation. Currently, an anti-cancer treatment scenario involving the imposition of stress on target cancer cells is gaining traction to augment or even replace conventional therapeutic regimens. Therefore, a comprehensive understanding of stress response pathways is crucial for devising and implementing novel therapeutic strategies.
Shun-Suke Sakai, Atsushi Hasegawa, Ryosuke Ishimura, Naoki Tamura, Shun Kageyama, Satoko Komatsu-Hirota, Manabu Abe, Yiwei Ling, Shujiro Okuda, Manabu Funayama, et al.
Molecular and Cellular Biology; https://doi.org/10.1128/mcb.00024-21

Abstract:
A germline copy number duplication of chromosome 14q32, which contains ATG2B and GSKIP , was identified in families with myeloproliferative neoplasm (MPN). Herein, we show that mice lacking both Atg2b and Gskip , but not either alone, exhibited decreased hematopoiesis, resulting in death in utero accompanied by anemia. In marked contrast to MPN patients with duplication of ATG2B and GSKIP , the number of hematopoietic stem cells (HSCs), in particular long-term HSCs, in double knockout fetal livers were significantly decreased due to increased cell death. Although the remaining HSCs still had the ability to differentiate into hematopoietic progenitor cells, the differentiation efficiency was quite low. Remarkably, mice with knockout of Atg2b or Gskip alone did not show any hematopoietic abnormality. Mechanistically, while loss of both genes had no effect on autophagy, it increased the expression of genes encoding enzymes involved in oxidative phosphorylation. Taken together, our results indicate that Atg2b and Gskip play a synergistic effect in maintaining the pool size of HSCs.
Megan McAleavy, Qian Zhang, Peter J. Ehmann, Jianing Xu, Matthew F. Wipperman, Dharani Ajithdoss, Li Pan, Matthew Wakai, Raphael Simonson, Abhilash Gadi, et al.
Molecular and Cellular Biology; https://doi.org/10.1128/mcb.00467-21

Abstract:
A subset of hospitalized COVID-19 patients, particularly the aged and those with co-morbidities, develop the most severe form of the disease, characterized by Acute Respiratory Disease Syndrome (ARDS), coincident with experiencing a “cytokine storm." Here, we demonstrate that cytokines which activate the NF-kappaB pathway can induce Activin A. Patients with elevated Activin A, Activin B, and FLRG at hospital admission were associated with the most severe outcomes of COVID-19, including the requirement for mechanical ventilation, and all-cause mortality. A prior study showed that Activin A could decrease viral load, which indicated there might be a risk to giving COVID-19 patients an inhibitor of Activin. To evaluate this, the role for Activin A was examined in a hamster model of SARS-CoV2 infection, via blockade of Activin A signaling. The hamster model demonstrated that use of an anti-ActivinA antibody did not worsen the disease and there was no evidence for increase in lung viral load and pathology. The study indicates blockade of Activin signaling may be beneficial in treating COVID-19 patients experiencing ARDS.
Peyman P. Aryanpur, Telsa M. Mittelmeier,
Molecular and Cellular Biology; https://doi.org/10.1128/mcb.00244-21

Abstract:
Ded1 is a conserved RNA helicase that promotes translation initiation in steady-state conditions. Ded1 has also been shown to regulate translation during cellular stress and affect the dynamics of stress granules (SGs), accumulations of RNA and protein linked to translation repression. To better understand its role in stress responses, we examined Ded1 function in two different models: DED1 overexpression and oxidative stress. DED1 overexpression inhibits growth and promotes the formation of SGs. A ded1 mutant lacking the low-complexity C-terminal region ( ded1-ΔCT ), which mediates Ded1 oligomerization and interaction with the translation factor eIF4G1, suppressed these phenotypes, consistent with other stresses. During oxidative stress, a ded1-ΔCT mutant was defective in growth and in SG formation compared to wild-type cells, although SGs were increased rather than decreased in these conditions. Unlike stress induced by direct TOR inhibition, the phenotypes in both models were only partially dependent on eIF4G1 interaction, suggesting an additional contribution from Ded1 oligomerization. Furthermore, examination of the growth defects and translational changes during oxidative stress suggested that Ded1 plays a role during recovery from stress. Integrating these disparate results, we propose that Ded1 controls multiple aspects of translation and RNP dynamics in both initial stress responses and during recovery.
Himangshu S. Bose, Randy M. Whittal, Curtis E. Lanier, Brendan Marshall, Maheshinie Rajapaksha, Brian W. Wheeler, Nicholas D. Carbo, Elin M. Hahn, Elizabeth W. Perry, Neal M. Hall, et al.
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00357-21

Abstract:
Estradiol is essential for the development of female sex characteristics and fertility. Postmenopausal women and breast cancer patients have high levels of estradiol.
Deborah P. Lavin, Leila Abassi, Mohammed Inayatullah,
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00183-21

Abstract:
The bHLH TF Mnt promotes epithelial to mesenchymal transition through epigenetic repression of the epithelial gene expression program.
Marina Dall’Osto, Laura Pierini, Nicolas Valery, , Marie-Jeanne Pillaire
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00090-21

Abstract:
DNA polymerase kappa (Pol κ) has been well documented thus far for its specialized DNA synthesis activity during translesion replication, progression of replication forks through regions difficult to replicate, restart of stalled forks, and replication checkpoint efficiency. Pol κ is also required for the stabilization of stalled forks, although the mechanisms are poorly understood.
Jaswinder Kaur,
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00233-21

Abstract:
Mitochondrial oxidative phosphorylation (OXPHOS) enzymes have a dual genetic origin. Mechanisms regulating the expression of nucleus-encoded OXPHOS subunits in response to metabolic cues (glucose versus glycerol) are well understood, while the regulation of mitochondrially encoded OXPHOS subunits is poorly defined. Here, we show that IRC3 , a DEAD/H box helicase gene, previously implicated in mitochondrial DNA maintenance, is central to integrating metabolic cues with mitochondrial translation.
Elizabeth L. Castle, Carolyn-Ann Robinson, Pauline Douglas, Kristina D. Rinker,
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00399-21

Abstract:
Processing bodies (PBs) are ribonucleoprotein granules important for cytokine mRNA decay that are targeted for disassembly by many viruses. Kaposi’s sarcoma-associated herpesvirus is the etiological agent of the inflammatory endothelial cancer, Kaposi’s sarcoma, and a PB-regulating virus.
Anqi Zhang, Takafumi Suzuki, Saki Adachi, Eriko Naganuma, Norio Suzuki, Tomonori Hosoya, Ken Itoh, Michael B. Sporn,
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00236-21

Abstract:
Heme oxygenase-1 (HO-1) is the key enzyme for heme catabolism and cytoprotection. Whereas HO-1 gene expression in response to various stresses has been investigated extensively, the precise mechanisms by which HO-1 gene expression is regulated by the HO-1 substrate heme remain elusive. To systematically examine whether stress-mediated induction and substrate-mediated induction of HO-1 utilize similar or distinct regulatory pathways, we developed an HO-1–DsRed-knock-in reporter mouse in which the HO-1 gene is floxed by loxP sites and the DsRed gene has been inserted.
Nicole J. Wayne, Katherine E. Dembny, Tyler Pease, Farrin Saba, Xiaohong Zhao, Daniel C. Masison, Lois E. Greene
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00122-21

Abstract:
The aggregation of huntingtin fragments with expanded polyglutamine repeat regions (HttpolyQ) that cause Huntington’s disease depends on the presence of a prion with an amyloid conformation in yeast. As a result of this relationship, HttpolyQ aggregation indirectly depends on Hsp104 due to its essential role in prion propagation.
Yoo Jin Joo,
Molecular and Cellular Biology; https://doi.org/10.1128/mcb.00373-21

Abstract:
In our previously published studies, RNA polymerase II transcription initiation complexes were assembled from yeast nuclear extracts onto immobilized transcription templates and analyzed by quantitative mass spectrometry. In addition to the expected basal factors and coactivators, we discovered that the uncharacterized protein Gds1/YOR355W showed activator-stimulated association with promoter DNA. Gds1 co-precipitated with the histone H4 acetyltransferase NuA4, and its levels often tracked with NuA4 in immobilized template experiments. GDS1 deletion led to reduction in H4 acetylation in vivo, and caused other phenotypes consistent with partial loss of NuA4 activity. Genome-wide chromatin immunoprecipitation revealed that the reduction in H4 acetylation was strongest at ribosomal protein gene promoters and other genes with high NuA4 occupancy. Therefore, while Gds1 is not a stoichiometric subunit of NuA4, we propose that it interacts with and modulates NuA4 in specific promoter contexts. Gds1 has no obvious metazoan homolog, but the Alphafold2 algorithm predicts that a section of Gds1 resembles the winged-helix/forkhead domain found in DNA-binding proteins such as the FOX transcription factors and histone H1.
Aiwen Jiang, Hongyun Guo, Liangliang Zhang, Xiaoyu Jiang, Xiying Zhang, Wangjun Wu, Honglin Liu
Molecular and Cellular Biology; https://doi.org/10.1128/mcb.00327-21

Abstract:
The activity of AMPKα is reduced in type-2 diabetes, and type-2 diabetes is associated with muscular atrophy. To date, there is little known about the mechanism by which FFA participates in muscular impairment. The purpose of the present study was to explore whether FFA damages myogenesis through AMPKα-HDAC4-miR-206 pathway. The results showed that 1mM FFA produced lipid accumulation, significantly impaired insulin signaling pathway and decreased myogenic differentiation of C2C12 myoblast cells. FFA reduced LKB1-AMPKα pathway; activation of AMPKα rescued the myogenic impairment caused by FFA ( P< 0.05). AMPKα promoted myogenesis by regulating the expression of miR-206 through HDAC4 ( P< 0.05); AMPKα affected cell cycle and cell proliferation to promote myogenesis by regulating miR-206 and miR-206’s target gene - cyclin D1. In addition, AICAR and HDAC4 siRNA promoted myogenic differentiation compared with FFA group; however, this positive effect was significantly down-regulated after transfection of miR-206 inhibitor. In summary, AMPKα plays positive roles in myogenic differentiation and myogenesis, and FFA decreased myogenic differentiation and myotubes formation through AMPKα-HDAC4-miR-206 pathway.
Priyanka Barman, Rwik Sen, Amala Kaja, Jannatul Ferdoush, Shalini Guha, Chhabi K. Govind,
Molecular and Cellular Biology; https://doi.org/10.1128/mcb.00368-21

Abstract:
San1 ubiquitin ligase is involved in nuclear protein quality control via its interaction with intrinsically disordered proteins for ubiquitylation and proteasomal degradation. Since several transcription/chromatin regulatory factors contain intrinsically disordered domains and can be inhibitory to transcription when in excess, San1 might be involved in transcription regulation. To address this, we analyzed the role of San1 in genome-wide association of TBP [that nucleates pre-initiation complex (PIC) formation for transcription initiation] and RNA polymerase II (Pol II). Our results reveal the roles of San1 in regulating TBP recruitment to the promoters and Pol II association with the coding sequences, and hence PIC formation and coordination of elongating Pol II, respectively. Consistently, transcription is altered in the absence of San1. Such transcriptional alteration is associated with impaired ubiquitylation and proteasomal degradation of Spt16 and gene association of Paf1, but not the incorporation of centromeric histone, Cse4, into the active genes in Δsan1 . Collectively, our results demonstrate distinct functions of a nuclear protein quality control factor in regulating the genome-wide PIC formation and elongating Pol II (and hence transcription), thus unraveling new gene regulatory mechanisms.
Yihong Huang, Shuo Zheng, Ying Lin, Liming Ke
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00609-20

Abstract:
Triple-negative breast cancer (TNBC) is an aggressive histological subtype of breast cancer. It has been reported that the circular RNA (circRNA) circ-ERBB2 (circBase identifier hsa_circ_0007766) is mainly distributed in the cytoplasm of TNBC cells and promotes the proliferation and invasion of TNBC cells.
Zhaoyuan Niu, Fengling Wang, Shihui Lv, Yingpin Lv, Ming Liu, Lei Fu, Yushuang Yao, Lingzhi Wang, Wei Lin, Fang Yuan
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00115-21

Abstract:
Long noncoding RNAs (lncRNAs) have key functions in modulating cervical cancer (CC) genesis and progression. This work focused on exploring lncRNA HNRNPU-AS1's function in CC and the underlying mechanism.
Koki Nojiri, Shuhei Fudetani, Ayami Arai, Takuya Kitamura, ,
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00352-21

Abstract:
Sjögren-Larsson syndrome (SLS) is an inherited neurocutaneous disorder whose causative gene encodes the fatty aldehyde dehydrogenase ALDH3A2. To date, the detailed molecular mechanism of the skin pathology of SLS has remained largely unclear.
Tao Yao, Lei Zhang, Ye Fu, Lina Yao, Chengjie Zhou, Guozhong Chen
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00332-21

Abstract:
Evidence exists reporting that saikosaponin-d can prevent experimental sepsis, and this study aims to illustrate the molecular events underlying its renoprotective effects on lipopolysaccharide (LPS)-induced renal inflammation simulating sepsis. Through network pharmacology analysis and bioinformatics analysis, we identified that saikosaponin-d may influence sepsis development by mediating TCF7.
Thomas Rivas, James A. Goodrich, Jennifer F. Kugel
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00171-21

Abstract:
Infection by herpes simplex virus 1 (HSV-1) impacts nearly all steps of host cell gene expression. The regulatory mechanisms by which this occurs, and the interplay between host and viral factors, have yet to be fully elucidated.
Susanne Bacher, Hilda Stekman, Carla M. Farah, Annika Karger, Michael Kracht,
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00081-21

Abstract:
Cullin-4 ubiquitin ligase (CRL4) complexes are differentially composed and highly dynamic protein assemblies that control many biological processes, including the global genome nucleotide excision repair (GG-NER) pathway. Here, we identified the kinase mitogen-activated protein kinase kinase kinase 1 (MEKK1) as a novel constitutive interactor of a cytosolic CRL4 complex that disassembles after DNA damage due to the caspase-mediated cleavage of MEKK1.
Katja Kratz, Mariela Artola-Borán, Saho Kobayashi-Era, Gene Koh, Goncalo Oliveira, Shunsuke Kobayashi, Andreia Oliveira, Xueqing Zou, Julia Richter, Masataka Tsuda, et al.
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00303-21

Abstract:
Germline mutations in the mismatch repair (MMR) genes MSH2 , MSH6 , MLH1 , and PMS2 are linked to cancer of the colon and other organs, characterized by microsatellite instability and a large increase in mutation frequency. Unexpectedly, mutations in EXO1 , encoding the only exonuclease genetically implicated in MMR, are not linked to familial cancer and cause a substantially weaker mutator phenotype.
Joyce van de Leemput,
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00185-21

Abstract:
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the COVID-19 pandemic, responsible for millions of deaths globally. Even with effective vaccines, SARS-CoV-2 will likely maintain a hold in the human population through gaps in efficacy and vaccination and arising new strains.
Pruthvi Gowda, Kirti Lathoria, Shalini Sharma, Shruti Patrick, Sonia B. Umdor,
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00449-20

Abstract:
A desynchronized circadian rhythm in tumors is coincident with aberrant inflammation and dysregulated metabolism. As their interrelationship in cancer etiology is largely unknown, we investigated the link among the three in glioma.
Azlann Arnett, Keagan G. Moo, Kaitlin J. Flynn, Thomas B. Sundberg, Liv Johannessen, Alykhan F. Shamji, Nathanael S. Gray, Thomas Decker, Ye Zheng, Vivian H. Gersuk, et al.
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00085-21

Abstract:
Immune health requires innate and adaptive immune cells to engage precisely balanced pro- and anti-inflammatory forces. We employ the concept of chemical immunophenotypes to classify small molecules functionally or mechanistically according to their patterns of effects on primary innate and adaptive immune cells.
Mingyang Li, Chunli Qi, RenXing Song, Chunming Xiong, Xiao Zhong, Ziguang Song, Zhongping Ning, Xiang Song
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00580-20

Abstract:
Cardiac fibrosis is a hallmark of various heart diseases and ultimately leads to heart failure. Although long noncoding RNA (lncRNA) SNHG20 has been reported to play important roles in various cancers, its function in cardiac fibrosis remains unclear.
Xinjun Ji, Anupama Jha, Jesse Humenik, Louis R. Ghanem, Andrew Kromer, Christopher Duncan-Lewis, Elizabeth Traxler, Mitchell J. Weiss, Yoseph Barash, Stephen A. Liebhaber
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00668-20

Abstract:
We previously demonstrated that the two paralogous RNA-binding proteins PCBP1 and PCBP2 are individually essential for mouse development: Pcbp1 -null embryos are peri-implantation lethal, while Pcbp2 -null embryos lose viability at midgestation. Midgestation Pcbp2 −/− embryos revealed a complex phenotype that included loss of certain hematopoietic determinants. Whether PCBP2 directly contributes to erythropoietic differentiation and whether PCBP1 has a role in this process remained undetermined.
Guanghua Qin, Xuejian Wu
Molecular and Cellular Biology, Volume 41; https://doi.org/10.1128/mcb.00100-21

Abstract:
Several studies have examined the relationship between osteosarcoma (OS) and microRNAs (miRNAs). However, only a few researchers have investigated the underlying mechanism of circular RNAs (circRNAs) in OS development.
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