journal
MENU ▼
Read by QxMD icon Read
search

Journal of Cell Biology

journal
https://www.readbyqxmd.com/read/28235948/erin-goley-catching-the-bug-for-studying-the-cytoskeleton
#1
Marie Anne O'Donnell
Erin Goley investigates how the microbial cytoskeleton controls cell growth and division.
February 24, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28235947/human-centromeric-cenp-a-chromatin-is-a-homotypic-octameric-nucleosome-at-all-cell-cycle-points
#2
Yael Nechemia-Arbely, Daniele Fachinetti, Karen H Miga, Nikolina Sekulic, Gautam V Soni, Dong Hyun Kim, Adeline K Wong, Ah Young Lee, Kristen Nguyen, Cees Dekker, Bing Ren, Ben E Black, Don W Cleveland
Chromatin assembled with centromere protein A (CENP-A) is the epigenetic mark of centromere identity. Using new reference models, we now identify sites of CENP-A and histone H3.1 binding within the megabase, α-satellite repeat-containing centromeres of 23 human chromosomes. The overwhelming majority (97%) of α-satellite DNA is found to be assembled with histone H3.1-containing nucleosomes with wrapped DNA termini. In both G1 and G2 cell cycle phases, the 2-4% of α-satellite assembled with CENP-A protects DNA lengths centered on 133 bp, consistent with octameric nucleosomes with DNA unwrapping at entry and exit...
February 24, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28235946/vhl-promotes-immune-response-against-renal-cell-carcinoma-via-nf-%C3%AE%C2%BAb-dependent-regulation-of-vcam-1
#3
David Labrousse-Arias, Emma Martínez-Alonso, María Corral-Escariz, Raquel Bienes-Martínez, Jaime Berridy, Leticia Serrano-Oviedo, Elisa Conde, María-Laura García-Bermejo, José M Giménez-Bachs, Antonio S Salinas-Sánchez, Ricardo Sánchez-Prieto, Masahiro Yao, Marina Lasa, María J Calzada
Vascular cell adhesion molecule 1 (VCAM-1) is an adhesion molecule assigned to the activated endothelium mediating immune cells adhesion and extravasation. However, its expression in renal carcinomas inversely correlates with tumor malignancy. Our experiments in clear cell renal cell carcinoma (ccRCC) cell lines demonstrated that von Hippel Lindau (VHL) loss, hypoxia, or PHD (for prolyl hydroxylase domain-containing proteins) inactivation decreased VCAM-1 levels through a transcriptional mechanism that was independent of the hypoxia-inducible factor and dependent on the nuclear factor κB signaling pathway...
February 24, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28235945/a-game-of-musical-chairs-pro-and-anti-resection-factors-compete-for-topbp1-binding-after-dna-damage
#4
Kenji Shimada, Susan M Gasser
DNA double strand breaks (DSBs) are generally repaired through nonhomologous end joining or homologous recombination. In this issue, Liu et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201607031) report that the conserved scaffold protein TOPBP1(Dpb11) provides binding sites for both pro- and anti-resection factors at DSBs, providing insights into repair pathway regulation.
February 24, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28228534/topbp1-dpb11-plays-a-conserved-role-in-homologous-recombination-dna-repair-through-the-coordinated-recruitment-of-53bp1-rad9
#5
Yi Liu, José Renato Cussiol, Diego Dibitetto, Jennie Rae Sims, Shyam Twayana, Robert Samuel Weiss, Raimundo Freire, Federica Marini, Achille Pellicioli, Marcus Bustamante Smolka
Genome maintenance and cancer suppression require homologous recombination (HR) DNA repair. In yeast and mammals, the scaffold protein TOPBP1(Dpb11) has been implicated in HR, although its precise function and mechanism of action remain elusive. In this study, we show that yeast Dpb11 plays an antagonistic role in recombination control through regulated protein interactions. Dpb11 mediates opposing roles in DNA end resection by coordinating both the stabilization and exclusion of Rad9 from DNA lesions. The Mec1 kinase promotes the pro-resection function of Dpb11 by mediating its interaction with the Slx4 scaffold...
February 22, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28228533/fragile-phagocytes-fmrp-positively-regulates-engulfment-activity
#6
Mary A Logan
Defective immune system function is implicated in autism spectrum disorders, including Fragile X syndrome. In this issue, O'Connor et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201607093) demonstrate that phagocytic activity of systemic immune cells is compromised in a Drosophila melanogaster model of Fragile X, highlighting intriguing new mechanistic connections between FMRP, innate immunity, and abnormal development.
February 22, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28223318/a-drosophila-model-of-fragile-x-syndrome-exhibits-defects-in-phagocytosis-by-innate-immune-cells
#7
Reed M O'Connor, Elizabeth F Stone, Charlotte R Wayne, Emily V Marcinkevicius, Matt Ulgherait, Rebecca Delventhal, Meghan M Pantalia, Vanessa M Hill, Clarice G Zhou, Sophie McAllister, Anna Chen, Jennifer S Ziegenfuss, Wesley B Grueber, Julie C Canman, Mimi M Shirasu-Hiza
Fragile X syndrome, the most common known monogenic cause of autism, results from the loss of FMR1, a conserved, ubiquitously expressed RNA-binding protein. Recent evidence suggests that Fragile X syndrome and other types of autism are associated with immune system defects. We found that Drosophila melanogaster Fmr1 mutants exhibit increased sensitivity to bacterial infection and decreased phagocytosis of bacteria by systemic immune cells. Using tissue-specific RNAi-mediated knockdown, we showed that Fmr1 plays a cell-autonomous role in the phagocytosis of bacteria...
February 21, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28213555/tubby-proteins-prove-their-adaptability
#8
Ben Short
Study reveals that Tubby family proteins help deliver GPCRs and other integral membrane proteins into cilia.
February 17, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28209645/retraction-the-dyrk-family-kinase-pom1-phosphorylates-the-f-bar-cdc15-to-prevent-division-at-cell-poles
#9
Pranav Ullal, Nathan A McDonald, Jun-Song Chen, Libera Lo Presti, Rachel H Roberts-Galbraith, Kathleen L Gould, Sophie G Martin
No abstract text is available yet for this article.
February 16, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28209644/mitochondrial-dysfunction-induces-dendritic-loss-via-eif2%C3%AE-phosphorylation
#10
Taiichi Tsuyama, Asako Tsubouchi, Tadao Usui, Hiromi Imamura, Tadashi Uemura
Mitochondria are key contributors to the etiology of diseases associated with neuromuscular defects or neurodegeneration. How changes in cellular metabolism specifically impact neuronal intracellular processes and cause neuropathological events is still unclear. We here dissect the molecular mechanism by which mitochondrial dysfunction induced by Prel aberrant function mediates selective dendritic loss in Drosophila melanogaster class IV dendritic arborization neurons. Using in vivo ATP imaging, we found that neuronal cellular ATP levels during development are not correlated with the progression of dendritic loss...
February 16, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28209643/eif2%C3%AE-links-mitochondrial-dysfunction-to-dendritic-degeneration
#11
Xin Qi
Although mitochondrial dysfunction has been associated with dendritic pathology in many neuronal types, how mitochondrial impairment causes the vulnerability of neuronal subtypes remains unknown. In this issue, Tsuyama et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201604065) identify eIF2α phosphorylation as a critical regulator of mitochondrial dysfunction-mediated selective dendritic loss in Drosophila neurons.
February 16, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28193702/the-peroxisomes-strike-bak-regulation-of-peroxisome-integrity-by-the-bcl-2-family
#12
Jerry Edward Chipuk, Mark P A Luna-Vargas
Within the mitochondrial pathway of apoptosis, VDAC2 controls both the localization and proapoptotic activity of BAK. In this issue, Hosoi et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201605002) find that loss of VDAC2 diverts BAK into peroxisome membranes, revealing the ability of BAK to control peroxisome membrane integrity and the release of soluble peroxisomal matrix proteins.
February 13, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28193701/osteoblastic-lrp4-promotes-osteoclastogenesis-by-regulating-atp-release-and-adenosine-a2ar-signaling
#13
Lei Xiong, Ji-Ung Jung, Hao-Han Guo, Jin-Xiu Pan, Xiang-Dong Sun, Lin Mei, Wen-Cheng Xiong
Bone homeostasis depends on the functional balance of osteoblasts (OBs) and osteoclasts (OCs). Lrp4 is a transmembrane protein that is mutated in patients with high bone mass. Loss of Lrp4 in OB-lineage cells increases bone mass by elevating bone formation by OBs and reducing bone resorption by OCs. However, it is unclear how Lrp4 deficiency in OBs impairs osteoclastogenesis. Here, we provide evidence that loss of Lrp4 in the OB lineage stabilizes the prorenin receptor (PRR) and increases PRR/V-ATPase-driven ATP release, thereby enhancing the production of the ATP derivative adenosine...
February 13, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28193700/the-nuclear-transport-receptor-importin-11-is-a-tumor-suppressor-that-maintains-pten-protein
#14
Muhan Chen, Dawid G Nowak, Navneet Narula, Brian Robinson, Kaitlin Watrud, Alexandra Ambrico, Tali M Herzka, Martha E Zeeman, Matthias Minderer, Wu Zheng, Saya H Ebbesen, Kendra S Plafker, Carlos Stahlhut, Victoria M Y Wang, Lorna Wills, Abu Nasar, Mireia Castillo-Martin, Carlos Cordon-Cardo, John E Wilkinson, Scott Powers, Raffaella Sordella, Nasser K Altorki, Vivek Mittal, Brendon M Stiles, Scott M Plafker, Lloyd C Trotman
Phosphatase and tensin homologue (PTEN) protein levels are critical for tumor suppression. However, the search for a recurrent cancer-associated gene alteration that causes PTEN degradation has remained futile. In this study, we show that Importin-11 (Ipo11) is a transport receptor for PTEN that is required to physically separate PTEN from elements of the PTEN degradation machinery. Mechanistically, we find that the E2 ubiquitin-conjugating enzyme and IPO11 cargo, UBE2E1, are limiting factors for PTEN degradation...
February 13, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28193699/importin-11-keeps-pten-safe-from-harm
#15
Nick R Leslie
In this issue, Chen et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201604025) show that Importin-11 traffics the tumor suppressor PTEN into the nucleus and in so doing protects it from cytoplasmic proteins that cause PTEN degradation. This work helps explain the nuclear accumulation of PTEN observed in many healthy tissues and, because Ipo11 mutant mice develop lung tumors, also implicates Importin-11 as a novel tumor suppressor.
February 13, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28188211/cluh-regulates-mitochondrial-metabolism-by-controlling-translation-and-decay-of-target-mrnas
#16
Désirée Schatton, David Pla-Martin, Marie-Charlotte Marx, Henriette Hansen, Arnaud Mourier, Ivan Nemazanyy, Alberto Pessia, Peter Zentis, Teresa Corona, Vangelis Kondylis, Esther Barth, Astrid C Schauss, Vidya Velagapudi, Elena I Rugarli
Mitochondria are essential organelles that host crucial metabolic pathways and produce adenosine triphosphate. The mitochondrial proteome is heterogeneous among tissues and can dynamically change in response to different metabolic conditions. Although the transcriptional programs that govern mitochondrial biogenesis and respiratory function are well known, posttranscriptional regulatory mechanisms remain unclear. In this study, we show that the cytosolic RNA-binding protein clustered mitochondria homologue (CLUH) regulates the expression of a mitochondrial protein network supporting key metabolic programs required under nutrient deprivation...
February 10, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28183718/the-heat-shock-factor-hsf1-juggles-protein-quality-control-and-metabolic-regulation
#17
Carles Cantó
Transcriptional regulators often act as central hubs to integrate multiple nutrient and stress signals. In this issue, Qiao et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201607091) demonstrate how heat shock factor 1 (HSF1) uncouples metabolic control from proteostatic regulation and unveils HSF1 as a critical transcriptional regulator of NAD(+) metabolism.
February 9, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28183717/the-transcriptional-regulator-of-the-chaperone-response-hsf1-controls-hepatic-bioenergetics-and-protein-homeostasis
#18
Aijun Qiao, Xiongjie Jin, Junfeng Pang, Demetrius Moskophidis, Nahid F Mivechi
Metabolic energy reprogramming facilitates adaptations to a variety of stress conditions and cellular dysfunction, but how the energetic demands are monitored and met in response to physiological stimuli remains elusive. Our data support a model demonstrating that heat shock factor 1 (HSF1), a master transcriptional regulator of the chaperone response, has been coopted from its role as a critical protein quality-control regulator to having a central role in systemic energy sensing and for metabolic adaptation to nutrient availability...
February 9, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28174205/the-vdac2-bak-axis-regulates-peroxisomal-membrane-permeability
#19
Ken-Ichiro Hosoi, Non Miyata, Satoru Mukai, Satomi Furuki, Kanji Okumoto, Emily H Cheng, Yukio Fujiki
Peroxisomal biogenesis disorders (PBDs) are fatal genetic diseases consisting of 14 complementation groups (CGs). We previously isolated a peroxisome-deficient Chinese hamster ovary cell mutant, ZP114, which belongs to none of these CGs. Using a functional screening strategy, VDAC2 was identified as rescuing the peroxisomal deficiency of ZP114 where VDAC2 expression was not detected. Interestingly, knockdown of BAK or overexpression of the BAK inhibitors BCL-XL and MCL-1 restored peroxisomal biogenesis in ZP114 cells...
February 7, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28174204/patterned-cell-and-matrix-dynamics-in-branching-morphogenesis
#20
REVIEW
Shaohe Wang, Rei Sekiguchi, William P Daley, Kenneth M Yamada
Many embryonic organs undergo branching morphogenesis to maximize their functional epithelial surface area. Branching morphogenesis requires the coordinated interplay of multiple types of cells with the extracellular matrix (ECM). During branching morphogenesis, new branches form by "budding" or "clefting." Cell migration, proliferation, rearrangement, deformation, and ECM dynamics have varied roles in driving budding versus clefting in different organs. Elongation of the newly formed branch and final maturation of the tip involve cellular mechanisms that include cell elongation, intercalation, convergent extension, proliferation, and differentiation...
February 7, 2017: Journal of Cell Biology
journal
journal
23805
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"