Physician

Internal Medicine

Richard Singer practices Internal Medicine. He went to medical school at David Geffen School of Medicine at UCLA. David Geffen School of Medicine at UCLA is one of the top medical schools in the US. David Geffen School of Medicine at UCLA is ranked 13/7 in Research/PrimaryCare. He over the years received 1 awards: "Meaningful Use Stage 1 Certification". Richard Singer is also published. He has 66 publications published. The lastest publication: "Retrograde transport from the yeast Golgi is mediated by two ARF GAP proteins with overlapping function.' He is registered with Medicare.

Publications

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• Dysregulated Arl1, a regulator of post-Golgi vesicle tethering, can inhibit endosomal transport and cell proliferation in yeast.
• The yeast Arf GTPase-activating protein Age1 is regulated by phospholipase D for post-Golgi vesicular transport.
• FACT, the Bur Kinase Pathway, and the Histone Co-Repressor HirC Have Overlapping Nucleosome-Related Roles in Yeast Transcription Elongation.
• Asf1 can promote trimethylation of H3 K36 by Set2.
• New mutant versions of yeast FACT subunit Spt16 affect cell integrity.
• The GAP domain and the SNARE, coatomer and cargo interaction region of the ArfGAP2/3 Glo3 are sufficient for Glo3 function.
• The Gcs1 Arf-GAP mediates Snc1,2 v-SNARE retrieval to the Golgi in yeast.
• Membrane metabolism mediated by Sec14 family members influences Arf GTPase activating protein activity for transport from the trans-Golgi.
• Domain organization of the yeast histone chaperone FACT: the conserved N-terminal domain of FACT subunit Spt16 mediates recovery from replication stress.
• The ArfGAP Glo3 is required for the generation of COPI vesicles.
• The FACT chromatin modulator: genetic and structure/function relationships.
• "Sleeping beauty": quiescence in Saccharomyces cerevisiae.
• Activity of specific lipid-regulated ADP ribosylation factor-GTPase-activating proteins is required for Sec14p-dependent Golgi secretory function in yeast.
• The Gcs1 and Age2 ArfGAP proteins provide overlapping essential function for transport from the yeast trans-Golgi network.
• A bipartite yeast SSRP1 analog comprised of Pob3 and Nhp6 proteins modulates transcription.
• Expression, analysis, and properties of yeast ADP-ribosylation factor (ARF) GTPase activating proteins (GAPs) Gcs1 and Glo3.
• Retrograde transport from the yeast Golgi is mediated by two ARF GAP proteins with overlapping function.
• The yeast protein complex containing cdc68 and pob3 mediates core-promoter repression through the cdc68 N-terminal domain.
• Characterization of the CP complex, an abundant dimer of Cdc68 and Pob3 proteins that regulates yeast transcriptional activation and chromatin repression.
• A yeast glutamine tRNA signals nitrogen status for regulation of dimorphic growth and sporulation.
• Prenylated isoforms of yeast casein kinase I, including the novel Yck3p, suppress the gcs1 blockage of cell proliferation from stationary phase.
• Saccharomyces cerevisiae Gcs1 is an ADP-ribosylation factor GTPase-activating protein.
• Sug1 modulates yeast transcription activation by Cdc68.
• Mutational analysis of the Prt1 protein subunit of yeast translation initiation factor 3.
• Mutations sensitizing yeast cells to the start inhibitor nalidixic acid.
• Efficient translation of an SSA1-derived heat-shock mRNA in yeast cells limited for cap-binding protein and eIF-4F.
• A member of a novel family of yeast ''zn-finger'' proteins mediates the transition from stationary phase to cell proliferation.
• Cell-cycle mutations among the collection of Saccharomyces cerevisiae dna mutants.
• The Saccharomyces cerevisiae Cdc68 transcription activator is antagonized by San1, a protein implicated in transcriptional silencing.
• An impaired RNA polymerase II activity in Saccharomyces cerevisiae causes cell-cycle inhibition at START.
• Yeast prt1 mutations alter heat-shock gene expression through transcript fragmentation.
• Stationary phase in the yeast Saccharomyces cerevisiae.
• Heat shock-mediated cell cycle blockage and G1 cyclin expression in the yeast Saccharomyces cerevisiae.
• Mitochondrial DNA loss by yeast reentry-mutant cells conditionally unable to proliferate from stationary phase.
• G1 cyclins regulate proliferation of the budding yeast Saccharomyces cerevisiae.
• CDC68, a yeast gene that affects regulation of cell proliferation and transcription, encodes a protein with a highly acidic carboxyl terminus.
• Expression of lacZ gene fusions affects downstream transcription in yeast.
• The Saccharomyces cerevisiae MYO2 gene encodes an essential myosin for vectorial transport of vesicles.
• The RSF1 gene regulates septum formation in Saccharomyces cerevisiae.
• The G1 interval in the mammalian cell cycle: dual control by mass accumulation and stage-specific activities.
• A cyclin protein modulates mitosis in the budding yeast Saccharomyces cerevisiae.
• Induction of yeast histone genes by stimulation of stationary-phase cells.
• Thermotolerance is independent of induction of the full spectrum of heat shock proteins and of cell cycle blockage in the yeast Saccharomyces cerevisiae.
• Genetic assessment of stationary phase for cells of the yeast Saccharomyces cerevisiae.
• Regulation of proliferation by the budding yeast Saccharomyces cerevisiae.
• Size selection identifies new genes that regulate Saccharomyces cerevisiae cell proliferation.
• Heat shock causes transient inhibition of yeast rRNA gene transcription.
• rRNA transcription initiation is decreased by inhibitors of the yeast cell cycle control step "start".
• Rapid initial cleavage of nascent pre-rRNA transcripts in yeast.
• Production of heat shock protein is independent of cell cycle blockage in the yeast Saccharomyces cerevisiae.
• A yeast mutant conditionally defective only for reentry into the mitotic cell cycle from stationary phase.
• Regulated arrest of cell proliferation mediated by yeast prt1 mutations.
• Molecular characterization of the yeast PRT1 gene in which mutations affect translation initiation and regulation of cell proliferation.
• Effects of sinefungin on rRNA production and methylation in the yeast Saccharomyces cerevisiae.
• Indirect suppression of the wee1 mutant phenotype in Schizosaccharomyces pombe.
• Novel cell cycle regulation in the yeast Schizosaccharomyces pombe. The DNA-division sequence modulates mass accumulation.
• Growth and the DNA-division sequence in the yeast Saccharomyces cerevisiae.
• Mating ability during chemically induced G1 arrest of cells of the yeast Saccharomyces cerevisiae.
• Bud formation by the yeast Saccharomyces cerevisiae is directly dependent on "start".
• Growth and the cell cycle of the yeast Saccharomyces cerevisiae. I. Slowing S phase or nuclear division decreases the G1 cell cycle period.
• Growth and the cell cycle of the yeast Saccharomyces cerevisiae. II. Relief of cell-cycle constraints allows accelerated cell divisions.
• Nature of the G1 phase of the yeast Saccharomyces cerevisiae.
• Ornithine decarboxylase activity and cell cycle regulation in Saccharomyces cerevisiae.
• Ribosomal precursor RNA metabolism and cell division in the yeast Saccharomyces cerevisiae.
• Transient cell cycle arrest of Saccharomyces cerevisiae by amino acid analog beta-2-DL-thienylalanine.

Schools

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• David Geffen School Of Medicine At UCLA University Of California Los Angeles

• Cedar Sinai

Doctors Specialties

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• Internal Medicine

Accepted Insurances

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Awards

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• Meaningful Use Stage 1 Certification

Education

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• Cedars-Sinai Medical Center
• David Geffen School of Medicine at UCLA

Drug Facts

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NPI NUMBER		1922009638
NPPES Provider LastName		SINGER
NPPES Provider FirstName		RICHARD
NPPES Provider ZIPCode		068805200
NPPES Provider State		CT
Specialty Description		Internal Medicine
Total Claim Count		2050.0
Distinct Opioid Count		7.0
Opioid Claim Count		169.0
Percent Opioid Claims		8.24

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Medicare Facts

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National Provider Identifier [NPI]	1922009638
Last Name Of The Provider	SINGER
First Name Of The Provider	RICHARD
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