Filter
Associated Lab
- Aguilera Castrejon Lab (14) Apply Aguilera Castrejon Lab filter
- Ahrens Lab (52) Apply Ahrens Lab filter
- Aso Lab (39) Apply Aso Lab filter
- Baker Lab (38) Apply Baker Lab filter
- Betzig Lab (110) Apply Betzig Lab filter
- Beyene Lab (9) Apply Beyene Lab filter
- Bock Lab (17) Apply Bock Lab filter
- Branson Lab (48) Apply Branson Lab filter
- Card Lab (38) Apply Card Lab filter
- Cardona Lab (63) Apply Cardona Lab filter
- Chklovskii Lab (13) Apply Chklovskii Lab filter
- Clapham Lab (11) Apply Clapham Lab filter
- Cui Lab (19) Apply Cui Lab filter
- Darshan Lab (12) Apply Darshan Lab filter
- Dennis Lab (1) Apply Dennis Lab filter
- Dickson Lab (46) Apply Dickson Lab filter
- Druckmann Lab (25) Apply Druckmann Lab filter
- Dudman Lab (46) Apply Dudman Lab filter
- Eddy/Rivas Lab (30) Apply Eddy/Rivas Lab filter
- Egnor Lab (11) Apply Egnor Lab filter
- Espinosa Medina Lab (16) Apply Espinosa Medina Lab filter
- Feliciano Lab (6) Apply Feliciano Lab filter
- Fetter Lab (41) Apply Fetter Lab filter
- Fitzgerald Lab (27) Apply Fitzgerald Lab filter
- Freeman Lab (15) Apply Freeman Lab filter
- Funke Lab (33) Apply Funke Lab filter
- Gonen Lab (91) Apply Gonen Lab filter
- Grigorieff Lab (62) Apply Grigorieff Lab filter
- Harris Lab (57) Apply Harris Lab filter
- Heberlein Lab (94) Apply Heberlein Lab filter
- Hermundstad Lab (21) Apply Hermundstad Lab filter
- Hess Lab (68) Apply Hess Lab filter
- Jayaraman Lab (43) Apply Jayaraman Lab filter
- Ji Lab (32) Apply Ji Lab filter
- Johnson Lab (6) Apply Johnson Lab filter
- Kainmueller Lab (19) Apply Kainmueller Lab filter
- Karpova Lab (14) Apply Karpova Lab filter
- Keleman Lab (13) Apply Keleman Lab filter
- Keller Lab (75) Apply Keller Lab filter
- Koay Lab (16) Apply Koay Lab filter
- Lavis Lab (131) Apply Lavis Lab filter
- Lee (Albert) Lab (34) Apply Lee (Albert) Lab filter
- Leonardo Lab (23) Apply Leonardo Lab filter
- Li Lab (25) Apply Li Lab filter
- Lippincott-Schwartz Lab (155) Apply Lippincott-Schwartz Lab filter
- Liu (Yin) Lab (5) Apply Liu (Yin) Lab filter
- Liu (Zhe) Lab (56) Apply Liu (Zhe) Lab filter
- Looger Lab (137) Apply Looger Lab filter
- Magee Lab (49) Apply Magee Lab filter
- Menon Lab (18) Apply Menon Lab filter
- Murphy Lab (13) Apply Murphy Lab filter
- O'Shea Lab (4) Apply O'Shea Lab filter
- Otopalik Lab (1) Apply Otopalik Lab filter
- Pachitariu Lab (38) Apply Pachitariu Lab filter
- Pastalkova Lab (18) Apply Pastalkova Lab filter
- Pavlopoulos Lab (19) Apply Pavlopoulos Lab filter
- Pedram Lab (12) Apply Pedram Lab filter
- Podgorski Lab (16) Apply Podgorski Lab filter
- Reiser Lab (48) Apply Reiser Lab filter
- Riddiford Lab (44) Apply Riddiford Lab filter
- Romani Lab (40) Apply Romani Lab filter
- Rubin Lab (138) Apply Rubin Lab filter
- Saalfeld Lab (58) Apply Saalfeld Lab filter
- Satou Lab (16) Apply Satou Lab filter
- Scheffer Lab (36) Apply Scheffer Lab filter
- Schreiter Lab (61) Apply Schreiter Lab filter
- Sgro Lab (20) Apply Sgro Lab filter
- Shroff Lab (18) Apply Shroff Lab filter
- Simpson Lab (23) Apply Simpson Lab filter
- Singer Lab (80) Apply Singer Lab filter
- Spruston Lab (91) Apply Spruston Lab filter
- Stern Lab (150) Apply Stern Lab filter
- Sternson Lab (54) Apply Sternson Lab filter
- Stringer Lab (24) Apply Stringer Lab filter
- Svoboda Lab (135) Apply Svoboda Lab filter
- Tebo Lab (30) Apply Tebo Lab filter
- Tervo Lab (9) Apply Tervo Lab filter
- Tillberg Lab (15) Apply Tillberg Lab filter
- Tjian Lab (64) Apply Tjian Lab filter
- Truman Lab (88) Apply Truman Lab filter
- Turaga Lab (46) Apply Turaga Lab filter
- Turner Lab (35) Apply Turner Lab filter
- Vale Lab (6) Apply Vale Lab filter
- Voigts Lab (1) Apply Voigts Lab filter
- Wang (Meng) Lab (6) Apply Wang (Meng) Lab filter
- Wang (Shaohe) Lab (20) Apply Wang (Shaohe) Lab filter
- Wu Lab (9) Apply Wu Lab filter
- Zlatic Lab (28) Apply Zlatic Lab filter
- Zuker Lab (25) Apply Zuker Lab filter
Associated Project Team
- CellMap (1) Apply CellMap filter
- COSEM (3) Apply COSEM filter
- Fly Descending Interneuron (10) Apply Fly Descending Interneuron filter
- Fly Functional Connectome (14) Apply Fly Functional Connectome filter
- Fly Olympiad (5) Apply Fly Olympiad filter
- FlyEM (48) Apply FlyEM filter
- FlyLight (45) Apply FlyLight filter
- GENIE (38) Apply GENIE filter
- Integrative Imaging (1) Apply Integrative Imaging filter
- Larval Olympiad (2) Apply Larval Olympiad filter
- MouseLight (16) Apply MouseLight filter
- NeuroSeq (1) Apply NeuroSeq filter
- ThalamoSeq (1) Apply ThalamoSeq filter
- Tool Translation Team (T3) (21) Apply Tool Translation Team (T3) filter
- Transcription Imaging (49) Apply Transcription Imaging filter
Publication Date
- 2024 (64) Apply 2024 filter
- 2023 (179) Apply 2023 filter
- 2022 (191) Apply 2022 filter
- 2021 (192) Apply 2021 filter
- 2020 (196) Apply 2020 filter
- 2019 (199) Apply 2019 filter
- 2018 (232) Apply 2018 filter
- 2017 (214) Apply 2017 filter
- 2016 (209) Apply 2016 filter
- 2015 (250) Apply 2015 filter
- 2014 (236) Apply 2014 filter
- 2013 (194) Apply 2013 filter
- 2012 (189) Apply 2012 filter
- 2011 (190) Apply 2011 filter
- 2010 (161) Apply 2010 filter
- 2009 (158) Apply 2009 filter
- 2008 (140) Apply 2008 filter
- 2007 (106) Apply 2007 filter
- 2006 (92) Apply 2006 filter
- 2005 (67) Apply 2005 filter
- 2004 (57) Apply 2004 filter
- 2003 (58) Apply 2003 filter
- 2002 (39) Apply 2002 filter
- 2001 (28) Apply 2001 filter
- 2000 (29) Apply 2000 filter
- 1999 (14) Apply 1999 filter
- 1998 (18) Apply 1998 filter
- 1997 (16) Apply 1997 filter
- 1996 (10) Apply 1996 filter
- 1995 (18) Apply 1995 filter
- 1994 (12) Apply 1994 filter
- 1993 (10) Apply 1993 filter
- 1992 (6) Apply 1992 filter
- 1991 (11) Apply 1991 filter
- 1990 (11) Apply 1990 filter
- 1989 (6) Apply 1989 filter
- 1988 (1) Apply 1988 filter
- 1987 (7) Apply 1987 filter
- 1986 (4) Apply 1986 filter
- 1985 (5) Apply 1985 filter
- 1984 (2) Apply 1984 filter
- 1983 (2) Apply 1983 filter
- 1982 (3) Apply 1982 filter
- 1981 (3) Apply 1981 filter
- 1980 (1) Apply 1980 filter
- 1979 (1) Apply 1979 filter
- 1976 (2) Apply 1976 filter
- 1973 (1) Apply 1973 filter
- 1970 (1) Apply 1970 filter
- 1967 (1) Apply 1967 filter
Type of Publication
3836 Publications
Showing 3601-3610 of 3836 resultsThe Roundabout (Robo) receptors have been intensively studied for their role in regulating axon guidance in the embryonic nervous system, whereas a role in dendritic guidance has not been explored. In the adult giant fiber system of Drosophila, we have revealed that ectopic Robo expression can regulate the growth and guidance of specific motor neuron dendrites, whereas Robo2 and Robo3 have no effect. We also show that the effect of Robo on dendritic guidance can be suppressed by Commissureless coexpression. Although we confirmed a role for all three Robo receptors in giant fiber axon guidance, the strong axon guidance alterations caused by overexpression of Robo2 or Robo3 have no effect on synaptic connectivity. In contrast, Robo overexpression in the giant fiber seems to directly interfere with synaptic function. We conclude that axon guidance, dendritic guidance, and synaptogenesis are separable processes and that the different Robo family members affect them distinctly.
Small molecules that alter protein function provide a means to modulate biological networks with temporal resolution. Here we demonstrate a potentially general and scalable method of identifying such molecules by application to a particular protein, Ure2p, which represses the transcription factors Gln3p and Nil1p. By probing a high-density microarray of small molecules generated by diversity-oriented synthesis with fluorescently labelled Ure2p, we performed 3,780 protein-binding assays in parallel and identified several compounds that bind Ure2p. One compound, which we call uretupamine, specifically activates a glucose-sensitive transcriptional pathway downstream of Ure2p. Whole-genome transcription profiling and chemical epistasis demonstrate the remarkable Ure2p specificity of uretupamine and its ability to modulate the glucose-sensitive subset of genes downstream of Ure2p. These results demonstrate that diversity-oriented synthesis and small-molecule microarrays can be used to identify small molecules that bind to a protein of interest, and that these small molecules can regulate specific functions of the protein.
Changes in synaptic connectivity patterns through the formation and elimination of dendritic spines may contribute to structural plasticity in the brain. We characterize this contribution quantitatively by estimating the number of different synaptic connectivity patterns attainable without major arbor remodeling. This number depends on the ratio of the synapses on a dendrite to the axons that pass within a spine length of that dendrite. We call this ratio the filling fraction and calculate it from geometrical analysis and anatomical data. The filling fraction is 0.26 in mouse neocortex, 0.22-0.34 in rat hippocampus. In the macaque visual cortex, the filling fraction increases by a factor of 1.6-1.8 from area V1 to areas V2, V4, and 7a. Since the filling fraction is much smaller than 1, spine remodeling can make a large contribution to structural plasticity.
The sense of taste provides animals with valuable information about the nature and quality of food. Mammals can recognize and respond to a diverse repertoire of chemical entities, including sugars, salts, acids and a wide range of toxic substances. Several amino acids taste sweet or delicious (umami) to humans, and are attractive to rodents and other animals. This is noteworthy because L-amino acids function as the building blocks of proteins, as biosynthetic precursors of many biologically relevant small molecules, and as metabolic fuel. Thus, having a taste pathway dedicated to their detection probably had significant evolutionary implications. Here we identify and characterize a mammalian amino-acid taste receptor. This receptor, T1R1+3, is a heteromer of the taste-specific T1R1 and T1R3 G-protein-coupled receptors. We demonstrate that T1R1 and T1R3 combine to function as a broadly tuned L-amino-acid sensor responding to most of the 20 standard amino acids, but not to their D-enantiomers or other compounds. We also show that sequence differences in T1R receptors within and between species (human and mouse) can significantly influence the selectivity and specificity of taste responses.
It is known that point mutations and rearrangements (deletions and duplications) of mammalian mitochondrial DNA (mtDNA) can result in mitochondrial dysfunction and human disease. Very little attention has been paid to mtDNA circular dimers (a complex form consisting of two genomes joined head-to-tail) despite their close association with human neoplasia. MtDNA dimers are frequently found in human leukemia, but the clinical relevance of their presence remains unknown. To begin to investigate the role of circular dimer mtDNA in the tumorigenic phenotype, we have created isogenic cell lines containing monomer and dimer mitochondrial genomes and compared the respective nuclear mRNA expression using Affymetrix gene array analysis. Surprisingly, a large number of nuclear gene changes were observed, with one of the largest category of genes being associated with remodeling of the cell surface and extracellular matrix. Since cell growth, migration, apoptosis, and many other cellular processes are influenced by signals initiating from the cell surface, the changes associated with the presence of mtDNA dimers could lead to significant alterations in tumorigenic potential and/or progression.
The homeodomain-containing transcription factor NKX3.1 is a putative prostate tumor suppressor that is expressed in a largely prostate-specific and androgen-regulated manner. Loss of NKX3.1 protein expression is common in human prostate carcinomas and prostatic intraepithelial neoplasia (PIN) lesions and correlates with tumor progression. Disruption of the murine Nkx3.1 gene results in defects in prostate branching morphogenesis, secretions, and growth. To more closely mimic the pattern of NKX3.1 loss that occurs in human prostate tumors, we have used Cre- and loxP-mediated recombination to delete the Nkx3.1 gene in the prostates of adult transgenic mice. Conditional deletion of one or both alleles of Nkx3.1 leads to the development of preinvasive lesions that resemble PIN. The pattern of expression of several biomarkers (Ki-67, E-cadherin, and high-molecular-weight cytokeratins) in these PIN lesions resembled that observed in human cases of PIN. Furthermore, PIN foci in mice with conditional deletion of a single Nkx3.1 allele lose expression of the wild-type allele. Our results support the role of NKX3.1 as a prostate tumor suppressor and indicate a role for this gene in tumor initiation.
The interaural time difference (ITD) is a major cue to sound localization along the horizontal plane. The maximum natural ITD occurs when a sound source is positioned opposite to one ear. We examined the ability of owls and humans to detect large ITDs in sounds presented through headphones. Stimuli consisted of either broad or narrow bands of Gaussian noise, 100 ms in duration. Using headphones allowed presentation of ITDs that are greater than the maximum natural ITD. Owls were able to discriminate a sound leading to the left ear from one leading to the right ear, for ITDs that are 5 times the maximum natural delay. Neural recordings from optic-tectum neurons, however, show that best ITDs are usually well within the natural range and are never as large as ITDs that are behaviorally discriminable. A model of binaural crosscorrelation with short delay lines is shown to explain behavioral detection of large ITDs. The model uses curved trajectories of a cross-correlation pattern as the basis for detection. These trajectories represent side peaks of neural ITD-tuning curves and successfully predict localization reversals by both owls and human subjects.
The principal regulator of p53 stability is HDM2, an E3 ligase that mediates p53 degradation via the ubiquitin-26S proteasome pathway. The current model holds that p53 degradation occurs exclusively on cytoplasmic proteasomes and hence has an absolute requirement for nuclear export of p53 via the CRM-1 pathway. However, proteasomes are abundant in both cytosol and nucleus, and no studies have been done to determine under what physiological circumstances p53 degradation might occur in the nucleus. We analyzed HDM2-mediated degradation of endogenous p53 in the presence of various nuclear export inhibitors of CRM-1, including leptomycin B (LMB), a noncompetitive, specific, and fast-acting inhibitor; and HTLV1-Rex protein, a potent competitive inhibitor. We found that significant HDM2-mediated p53 degradation took place in the presence of LMB or HTLV1-Rex, indicating that endogenous p53 degradation occurs locally in the nucleus, in parallel to cytoplasmic degradation. Moreover, p53 null cells that coexpressed export-defective mutants of p53 and HDM2 retained partial competence for p53 degradation. It is important that nuclear degradation of p53 occurred during the poststress recovery phase of a p53 response, after DNA damage ceased. We propose that the capability of local p53 degradation within the nucleus provides a tighter and faster control during the down-regulatory phase, when an active p53 program needs to be turned off quickly.
Axon bifurcation results in the formation of sister branches, and divergent segregation of the sister branches is essential for efficient innervation of multiple targets. From a genetic mosaic screen, we find that a lethal mutation in the Drosophila Down syndrome cell adhesion molecule (Dscam) specifically perturbs segregation of axonal branches in the mushroom bodies. Single axon analysis further reveals that Dscam mutant axons generate additional branches, which randomly segregate among the available targets. Moreover, when only one target remains, branching is suppressed in wild-type axons while Dscam mutant axons still form multiple branches at the original bifurcation point. Taken together, we conclude that Dscam controls axon branching and guidance such that a neuron can innervate multiple targets with minimal branching.