Unmet needs for HIV ancillary care services by healthcare coverage and Ryan White HIV/AIDS program assistance.

Objective: To investigate unmet needs for HIV ancillary care services by healthcare coverage type and Ryan White HIV/AIDS Program (RWHAP) assistance among adults with HIV.

Design: We analyzed data using the 2017-2019 cycles of the CDC Medical Monitoring Project, an annual, cross-sectional study designed to produce nationally representative estimates of characteristics among adults with diagnosed HIV.

Methods: Unmet need was defined as needing, but not receiving, one or more HIV ancillary care services.

The Role of Government-Funded Assistance Programs on HIV Testing Among Poor U.S. Adults.

Government-funded assistance program enrollment may play an important role in the overall increase of HIV testing among low-income U.S. adults.

Human genetic variants disrupt RGS14 nuclear shuttling and regulation of LTP in hippocampal neurons.

The human genome contains vast genetic diversity as naturally occurring coding variants, yet the impact of these variants on protein function and physiology is poorly understood. RGS14 is a multifunctional signaling protein that suppresses synaptic plasticity in dendritic spines of hippocampal neurons. RGS14 also is a nucleocytoplasmic shuttling protein, suggesting that balanced nuclear import/export and dendritic spine localization are essential for RGS14 functions.

Disability among adults with diagnosed HIV in the United States, 2017.

In the United States, one in four adults is living with a disability. Age-related changes, disease-related pathology and treatments can place a person with HIV at risk for a disability. We analyzed nationally representative data to describe disability status among adults ≥18 years with diagnosed HIV in the United States and Puerto Rico by demographic characteristics, health behaviors, quality of care, clinical outcomes and mental health status.

Depression Prevalence, Antidepressant Treatment Status, and Association with Sustained HIV Viral Suppression Among Adults Living with HIV in Care in the United States, 2009-2014.

Previous research indicates a high burden of depression among adults living with HIV and an association between depression and poor HIV clinical outcomes. National estimates of diagnosed depression, depression treatment status, and association with HIV clinical outcomes are lacking. We used 2009-2014 data from the Medical Monitoring Project to estimate diagnosed depression, antidepressant treatment status, and associations with sustained viral suppression (all viral loads in past year < 200 copies/mL).

Non-persistence to antiretroviral therapy among adults receiving HIV medical care in the United States.

Not taking medicine over a specific period of time-non-persistence to antiretroviral therapy (ART)-may be associated with higher HIV-viral load. However, national estimates of non-persistence among U.S.

Cell-type specific role of the RNA-binding protein, NONO, in the DNA double-strand break response in the mouse testes.

The tandem RNA recognition motif protein, NONO, was previously identified as a candidate DNA double-strand break (DSB) repair factor in a biochemical screen for proteins with end-joining stimulatory activity. Subsequent work showed that NONO and its binding partner, SFPQ, have many of the properties expected for bona fide repair factors in cell-based assays. Their contribution to the DNA damage response in intact tissue in vivo has not, however, been demonstrated.

Double-strand break repair deficiency in NONO knockout murine embryonic fibroblasts and compensation by spontaneous upregulation of the PSPC1 paralog.

NONO, SFPQ and PSPC1 make up a family of proteins with diverse roles in transcription, RNA processing and DNA double-strand break (DSB) repair. To understand long-term effects of loss of NONO, we characterized murine embryonic fibroblasts (MEFs) from knockout mice. In the absence of genotoxic stress, wild-type and mutant MEFs showed similar growth rates and cell cycle distributions, and the mutants were only mildly radiosensitive.

The mRNA-binding protein Zfp36 is upregulated by β-adrenergic stimulation and represses IL-6 production in 3T3-L1 adipocytes.

Obesity produces a chronic inflammatory state that contributes to the development of diabetes and atherosclerosis. In obese humans, fat depot adipocytes and macrophages produce inflammatory cytokines and other factors which exert unfavorable local and systemic immune responses. The expression of many cytokines is modulated at the post-transcriptional level by mRNA-binding proteins which recognize AU-rich elements (AREs) in the 3'-untranslated regions (3'-UTR) of these transcripts.

Intercalation of XR5944 with the estrogen response element is modulated by the tri-nucleotide spacer sequence between half-sites.

DNA-intercalating molecules can impair DNA replication, DNA repair, and gene transcription. We previously demonstrated that XR5944, a DNA bis-intercalator, specifically blocks binding of estrogen receptor-α (ERα) to the consensus estrogen response element (ERE). The consensus ERE sequence is AGGTCAnnnTGACCT, where nnn is known as the tri-nucleotide spacer.

Activation of the regulator of G protein signaling 14-Gαi1-GDP signaling complex is regulated by resistance to inhibitors of cholinesterase-8A.

RGS14 is a brain scaffolding protein that integrates G protein and MAP kinase signaling pathways. Like other RGS proteins, RGS14 is a GTPase activating protein (GAP) that terminates Gαi/o signaling. Unlike other RGS proteins, RGS14 also contains a G protein regulatory (also known as GoLoco) domain that binds Gαi1/3-GDP in cells and in vitro.

The tri-nucleotide spacer sequence between estrogen response element half-sites is conserved and modulates ERalpha-mediated transcriptional responses.

The estrogen response element (ERE) consensus sequence is AGGTCAnnnTGACCT, where nnn is known as the tri-nucleotide spacer sequence. Studying 1017 high-confidence ERalpha-bound loci, we found that genomic EREs are enriched for spacers composed of C(A/T)G, suggesting that the spacer may influence receptor binding and transcriptional responses. We designed consensus EREs containing variable spacer sequences and compared ERalpha binding in gel shift assays and enhancer function in reporter assays.

Location analysis for the estrogen receptor-alpha reveals binding to diverse ERE sequences and widespread binding within repetitive DNA elements.

Location analysis for estrogen receptor-alpha (ERalpha)-bound cis-regulatory elements was determined in MCF7 cells using chromatin immunoprecipitation (ChIP)-on-chip. Here, we present the estrogen response element (ERE) sequences that were identified at ERalpha-bound loci and quantify the incidence of ERE sequences under two stringencies of detection: <10% and 10-20% nucleotide deviation from the canonical ERE sequence. We demonstrate that approximately 50% of all ERalpha-bound loci do not have a discernable ERE and show that most ERalpha-bound EREs are not perfect consensus EREs.

RGS14 is a multifunctional scaffold that integrates G protein and Ras/Raf MAPkinase signalling pathways.

MAPkinase signalling is essential for cell growth, differentiation and cell physiology. G proteins and tyrosine kinase receptors each modulate MAPkinase signalling through distinct pathways. We report here that RGS14 is an integrator of G protein and MAPKinase signalling pathways.

Selective interactions between Gi alpha1 and Gi alpha3 and the GoLoco/GPR domain of RGS14 influence its dynamic subcellular localization.

RGS14 is a multifunctional protein that contains an RGS domain, which binds active Gi/o alpha-GTP, a GoLoco/GPR domain, which binds inactive Gi alpha-GDP, and a tandem Rap1/2 binding domain (RBD). Studies were initiated to determine the roles of these domains and their interactions with Gi alpha on RGS14 subcellular localization. We report that RGS14 dynamic subcellular localization in HeLa cells depends on distinct domains and selective interactions with preferred Gi alpha isoforms.

Human aurora-B binds to a proteasome alpha-subunit HC8 and undergoes degradation in a proteasome-dependent manner.

Human Aurora/Ipl1-related kinase 2 (Aurora-B) is a key regulator of mitosis. Here human proteasome alpha-subunit C8 (HC8) was identified to interact with the Aurora-B by yeast two-hybrid screen. This finding was confirmed by GST pull-down assays and immunoprecipitation experiments.