Search Grants — Free, No Account Required

NCI - National Cancer Institute

PROJECT SUMMARY Nearly 25% of cancers carry mutations in genes encoding components of SWI/SNF chromatin remodeling complexes, making SWI/SNF the most frequently mutated epigenetic regulator in cancer. SWI/SNF complexes facilitate lineage-specific gene expression by repositioning nucleosomes to enable transcription factor binding and by antagonizing the Polycomb repressive complexes (PRC2). Key to its function is heterogeneity of SWI/SNF complex composition, driven by unique subunits that define each of the three SWI/SNF sub-complex families and incorporation of mutually exclusive paralog proteins at several positions in the complex, which confers specificity of interaction with different transcription factors and histone modifications. Mutations that disrupt SWI/SNF function perturb complex integrity, disrupt PRC2 antagonism, and impair lineage- specific gene expression, which in susceptible progenitor cell contexts promotes oncogenic transformation. Despite key roles of SWI/SNF in controlling cell fate and frequent mutations of genes encoding SWI/SNF subunits in cancer, the mechanisms that control SWI/SNF function are poorly understood. The Roberts Lab recently published that the little-studied E3-ubiquitin ligase adaptor protein, DCAF5, is a specific dependency in Rhabdoid Tumors (RT) cells, which are driven by lack of SWI/SNF subunit SMARCB1. This work showed that DCAF5 promotes the highly proliferative, cancerous cell state by degrading residual SWI/SNF complexes, thereby preventing activation of lineage-specifying genes. This study established DCAF5 as a compelling therapeutic target and drug discovery efforts are now underway. Despite being ubiquitously expressed and evolutionarily conserved, the role of DCAF5 in regulating SWI/SNF function in normal cells is unknown. This proposal aims to define how DCAF5 controls SWI/SNF complex composition and function in non- malignant cells, using biochemical and computational approaches in cell models derived from a conditional Dcaf5 mouse model. This proposal directly supports the applicant’s training goals by providing training and mentorship to perform rigorous experiments to systematically dissect complex biological problems, acquire computational skills for integrative analyses of genomic data, and provides ample opportunities to enhance mentorship skills and build a strong scientific network. This applicant is supported by a world-class research institute with state- of-the-art resources, a collaborative laboratory, a dedicated sponsor with an impressive record of training early- career scientists, and collaborators with additional expertise required to achieve the applicant’s training goals. Together, this proposal supports the applicant’s long-term goal to learn to rigorously interrogate impactful scientific questions as an independent investigator and will reveal novel mechanisms that control SWI/SNF complex activity, which is critical for understanding both the mechanisms by which SWI/SNF dysregulation drives cancer and the consequences of therapeutic targeting of DCAF5.

NCI - National Cancer Institute

Small cell lung cancer (SCLC) is a highly aggressive, recalcitrant neuroendocrine carcinoma associated with a dismal prognosis. Despite recent progress, the molecular mechanisms that promote the development of SCLC remain incompletely delineated and there is an urgent need for refined, more effective therapies. Our long-term goal is to elucidate the chromatin, epigenetic and transcriptional mechanisms that promote and are required for SCLC, and to translate these mechanistic findings to the clinic. We have recently identified recurrent inactivating mutations in genes that encode for subunits of the polybromo-associated BAF (PBAF), a SWI/SNF chromatin remodeling complex. Yet, the functional consequences, underlying mechanisms and therapeutic targets associated with PBAF inactivation are unknown. Our project is based on the following preliminary findings: 1) Genomic analyses of ~1200 SCLC patient samples reveal recurrent loss of function mutations in PBAF. 2) PBAF exerts tumor suppressor functions in cellular models. 3) PBAF-deficiency leads to a marked acceleration of SCLC development and a stark reduction in overall survival. 4) PBAF-deficient SCLC models exhibit increased chromatin accessibility and an upregulation of pro-growth, pro-metastatic gene expression programs. 5) PBAFdeficient SCLCs are reliant on residual SWI/SNF complexes for growth. Altogether, our results pinpoint a critical function for PBAF in SCLC. Our central hypothesis is that PBAF-deficiency promotes SCLC development by altering chromatin structure, transcription factor binding and gene expression programs, and that such alterations lead to the development of SCLCs with unique biological features and therapeutic vulnerabilities. To test these hypotheses, we will pursue the following three aims: 1) Establish the functional importance of PBAF during SCLC initiation, progression, and metastasis. 2) Elucidate the transcriptional and epigenetic mechanisms underlying PBAF-deficient SCLCs. 3) Evaluate SWI/SNF inhibition as a therapeutic strategy for PBAF mutant SCLCs. This project is significant because it focuses on understanding the function of a recurrently mutated chromatin remodeling complex in SCLC and will guide future translational efforts for the most aggressive form of lung cancer. It is conceptually and mechanistically innovative because it leverages the first PBAF-deficient mouse model of SCLC. Our investigations require the use of these innovative animal models to study the functions of PBAF during SCLC initiation, progression and metastasis, which is currently not possible with any other model. While there is no equivalent non-animal alternative that allows us to effectively perform the proposed investigations, the animal studies will be complemented, when suitable, with human centric models such as ex vivo human systems, patient derived xenograft models (PDXs) and human SCLC specimens. Finally, our study is technically innovative as it implements state-of-the-art epigenomic profiling techniques. Collectively, our research will improve the understanding of SCLC biology and reveal new therapeutic avenues for patients.

NICHD - Eunice Kennedy Shriver National Institute of Child Health and Human Development

SUMMARY Human milk provides nutrients and important non-nutritive factors for infants that promote growth, development, and protection from infection1,2. Therefore, the World Health Organization (WHO) recommends exclusive breastfeeding for 6 months, then combining breastfeeding with solid foods for 18 months3. Lactation disorders reduce breastfeeding rates, and negatively impact both mothers and children. In mothers, lactation disorders influence mood and maternal well-being, while in children, they affect cognitive and socio-emotional development4, and can cause malnutrition, hypernatremia, hypoglycemia, and death5. Moreover, breastfeeding rates are lower in some ethnic minorities, which may partially reflect poor access to lactation consultants and early initiation of infant formula. Lactation disorders that specifically impair milk production and secretion affect about ~40% of breastfeeding mothers, the major phenotypes including: (i) agalactia: complete absence of milk secretion following birth; and (ii) hypogalactia: insufficient volume for optimal infant nutrition6,7. While post-partum stress, obesity, diabetes, and socioeconomic considerations have been associated with hypogalactia, we and others have demonstrated that hypogalactia has an inherited maternal genetic component6,8,9,10. However, the genetic mechanisms responsible for human lactation disorders are mostly unknown and have not yet been extensively investigated. We hypothesize that variations in genes involved in human milk production and secretion underlie disorders of milk production and secretion, and that these variants and genes can be discovered by interrogating genomic and extensive health and metadata from women with lactation disorders cases compared to unaffected female controls. We therefore propose to conduct a comprehensive study on whole exome sequencing (WES) data of lactation disorders patients. We are uniquely positioned to perform the first such study with the largest lactation disorders cohort to date (1,382 patients and over 60,000 female controls), combining four major biobanks: Vanderbilt University’s BioVU11,12, Mount Sinai Hospital’s BioMe Biobank13,14, All of Us and UK Biobank15,16. We propose a rigorous pipeline combining various state-of-the-art with cutting-edge approaches developed by us and others to: (1) obtain a high-quality WES lactation disorders cohort by variant- and sample-level quality control (QC)17,18, annotations19, and impact predictions20-22; (2) perform computational case-control analyses for high impact variants23,24; (3) prioritize variants and genes by biological relatedness approaches25-27 and use a novel quad-culture organotypic mammary gland model to characterize the molecular pathology of high impact variants; and (4) perform phenome-wide association studies (PheWAS)28 and polygenic risk score (PRS) analyses29. We expect that our findings of human lactation disorders genetics will be vital for understanding the physiology and pathophysiology of human milk systems, directly informing maternal, perinatal, neonatal health decisions, and ultimately guiding precision medicine approaches to improve women’s health.

NHLBI - National Heart Lung and Blood Institute

Project summary/Abstract Epigenetic regulation is crucial for directing the intricate processes of heart development, and the disruption of these precise mechanisms underlies various congenital heart defects. Epigenetic mechanisms, such as histone modifications, play key roles in coordinating gene expression programs that guide early lineage specification and differentiation. Lysine-specific histone demethylase 1 (LSD1) is a critical epigenetic regulator that removes mono- and di-methyl groups from histone H3 lysine 4 (H3K4me1/2), thereby influencing chromatin accessibility and transcriptional activity. Beyond its enzymatic function, LSD1 also acts as a scaffold that coordinates transcription factors and chromatin remodelers. However, how these distinct functions of LSD1 contribute to cardiac lineage specification remains poorly understood. Studies have shown that LSD1 is essential for embryonic survival, and recent mouse models have revealed specific developmental cardiac defects in the absence of LSD1. For example, LSD1 hypomorphic mice with impaired protein-protein interactions exhibit ventricular septal defects and perinatal lethality. Additionally, cardiomyocyte-specific LSD1 knockout embryos display reduced heart size, dilation, and embryonic lethality, indicating that LSD1 is necessary at multiple developmental stages in specific tissues. Our lab has further shown that LSD1 knockout embryonic stem cells (ESCs) fail to generate mesoderm and endoderm, instead favoring neuroectodermal fates. Importantly, while the loss of LSD1’s catalytic activity impairs cardiac differentiation, complete loss of LSD1 fully blocks it, emphasizing the significance of its non- catalytic functions in early cell fate decisions. In this proposal, I aim to unveil the precise role and molecular mechanism of LSD1 in regulating cardiac specification and heart development. I will use in vitro and in vivo models to dissect the role of LSD1 in cardiac development. State-of-the-art approaches such as CRISPR/Cas9 guided genome engineering, novel animal models, epigenomics, and single-cell RNA-seq will be used to address the central question. This project will clarify how LSD1 regulates early cell fate decisions in cardiac development, with long-term implications for understanding congenital heart defects and advancing epigenetic-targeted therapies.

NIAMS - National Institute of Arthritis and Musculoskeletal and Skin Diseases

Retrotransposons are interspersed genomic repeats that constitute almost half of the mammalian genome. Largely residing in the heterochromatin, retrotransposons are transiently induced during early development to regulate lineage differentiation, and kept silenced in adult terminally differentiated tissues. However, in human diseases such as cancer and aging, retrotransposons often exhibit aberrantly elevated activities, whose underlying molecular trigger and functional consequences are less understood. Murine skin represents an excellent model to study retrotransposon silencing mechanisms. As our largest organ, skin harbors highly abundant, well characterized, and genetically accessible adult stem cells. Hair follicle stem cells reside in an anatomically distinct niche known as the bulge, alternating between quiescence and activation in a synchronized fashion to fuel cyclic bouts of hair growth. Over repeated insults, hair follicle stem undergo functional exhaustion, the molecular driving events of which were often unclear. In the current proposal, I plan to examine chromatin regulators that couple adult stem cell activation with retrotransposon suppression during adult skin and hair follicle regenerations. Two central heterochromatin pathways are known to silence retrotransposons: tri-methylation on histone 3 lysine 9 (H3K9), catalyzed by histone lysine methyltransferases (KMTs), and DNA cytosine methylation, catalyzed by DNA methyltransferases (DNMTs). Moreover, lineage gene expression during stem cell differentiation depends on DNA demethylation, catalyzed by the DNA demethylase ten-eleven translocation (TET). While TETs are crucial for DNA methylome remodeling in early development, their regulations of retrotransposons in adult tissues remain underexplored. My preliminary analysis of genetic models in which the endogenous retroviruses (ERVs, a type of retrotransposons), are reactivated to drive skin stem cell exhaustion and hair loss, afforded me a unique tool to tackle these questions. Specifically, my prelim data indicated that a critical signal connecting TET to H3K9 KMT and DNMT function is the post-translational modification known as O-linked-β-N-acetylglucosamine (O-GlcNAc). I hypothesize that OGlcNAc catalyzed by the OGlcNAc transferase (OGT) is essential to suppress ERVs by interacting with H3K9 KMT and DNMT in the skin. I will examine OGT-deficient skin phenotypes and O-GlcNAc changes upon ERV reactivation, and dissect the mechanisms of OGlcNAc-orchestrated ERV suppressions. Study proposed here leverage my previous training in mouse genetics, development, epigenetics, and skin biology, and are designed to further train me with the state-of-art technologies such as CRISPR and classic methodologies in biochemistry and molecular biology. My training plan and my sponsor/co-sponsor support have been tailored to further foster my critical thinking, scientific communication, leadership and career development goals within MDACC and GSBS training environment. The proposed study, if successful, will provide important mechanistic insights into retrotransposon biology in adult skin, and mature me into an independent researcher.

NICHD - Eunice Kennedy Shriver National Institute of Child Health and Human Development

PROJECT SUMMARY More than 39.9 million people are living with HIV worldwide, including 1.2 million women who become pregnant annually. Suppressive antiretroviral therapy (ART) to pregnant women with HIV (WHIV) has been highly successful in reducing the number of new pediatric infections. However, HIV/ART exposure in utero and infancy can lead to reduced early life growth predisposing children for lifelong metabolic disease risk, so understanding adverse effects of HIV/ART exposure on infants is critical to protect millions of children worldwide. Human milk (HM) is essential for early infant metabolic health, and breastfeeding is recommended globally for WHIV on ART. However, HM is a complex mixture that is highly dependent on the maternal environment and HM components may influence child health. HM is rich in extracellular vesicles (EVs), nano-sized packages that survive digestion to deliver their bioactive cargoes. EV miRNAs (small noncoding RNAs) and metabolites (small polar metabolites and lipids) are important bioactive molecules that hold promise as drivers of these effects. Our goal is to investigate the role of maternal HIV/ART exposure on the HM EV-metabolome and EV-miRNAs and their subsequent impacts on child growth and body composition. To address this, we propose to leverage the Africa-based Obesogenic oRigins of maternal and Child metabolic Health Involving Dolutegravir (ORCHID) study of pregnant WHIV receiving tenofovir + lamivudine + dolutegravir (TLD) and HIV-seronegative pregnant women and their children (analyzing a subset, N=500; 250/group). Using anthropometry at 1, 2, 3, 6, 12 and 24 months of age and gold standard air displacement plethysmography to assess body composition, we will construct trajectories of overall infant growth and adiposity. In HM samples collected at 1 and 3 months postpartum, we will evaluate EV-miRNA expression with next-generation sequencing and the HM EV-metabolome with ultrasensitive metabolomics and lipidomics to address the following aims: Aim 1. Assess the association of maternal HIV/ART exposure with the human milk EV-metabolome and EV-miRNA across lactation; Aim 2. Investigate the associations of the human milk EV-metabolome and EV-miRNA with child growth; and Exploratory Aim 3. Develop a predictive multi-omic fingerprint of milk EV cargoes that can be used to identify HIV-exposed uninfected children (CHEU) with elevated risk of reduced growth and adiposity. Using machine learning approaches that account for joint effects and interactions, we will characterize miRNA-metabolome profiles in combination with traditional risk factors that identify children with elevated metabolic risk due to HIV/ART exposure during breastfeeding. With more than 1 million WHIV becoming pregnant each year and increasing numbers of children being exposed to HIV/ART through breastfeeding, our work will provide critical knowledge on how HIV/ART exposure impacts breastmilk composition and maternal-child communication to affect child health, providing key insights on nutrition and future targets for intervention and prevention.

NCI - National Cancer Institute

SUMMARY ABSTRACT: Cancer stem cells (CSCs) are a small population of cancer cells that are typically quiescent, but capable of self- renewal and tumor initiation. Non-CSCs, which make up the majority of the cancer cell population, are cells that are constantly dividing. Since CSCs are non-dividing, they are resistant to standard chemotherapy and radiation therapy, which only target actively dividing cells. Persistence of CSCs after therapy can thus result in disease relapse. Importantly, our recent work showed that programs of stemness are activated in tumor cells as they disseminate from primary tumors. Therefore, understanding what influences the formation of disseminating CSCs may provide new potential targets for therapeutic interventions of metastasis. Metastasis is a multi-step process and, in each step, disseminating tumor cells (DTCs) encounter different physical constrictions (e.g., physical confinement, solid stress, matrix stiffness, interstitial fluid pressure, and shear stress) that may affect their behavior. Recent reports in the literature indicate that one pathway for induction of programs of stemness is through the YAP/TAZ mechanotransduction signaling pathway, indicating that physical forces may, in part, be responsible for the induction of stemness in DTCs. This project will investigate the role physical constriction plays in stem cell induction by modelling the different physical constrictions that DTCs experience as they disseminate from primary tumors. This project will draw upon engineering and biological sciences to combine a unique, validated, fluorescent biosensor for stemness with advanced microfabricated microfluidic in vitro assays, and state-of-the-art intravital imaging of the live murine lung. We propose to use this combination to study the influence of physical forces on the selection, induction, and/or sustainment of metastasizing cancer stem cells, and evaluate their retention, survival, and extravasation efficiency in the in vivo lung.

Iowa Arts Council

Supports arts education projects in Iowa schools and communities, funding artist residencies, professional development for educators, and programs that integrate arts learning across the K-12 curriculum.

Iowa Arts Council

The Iowa Arts Council provides operating support grants to Iowa arts organizations, funding programming, staff, and operations that deliver arts and cultural experiences across the state's communities.

NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY The antisense gene asp maps in the HIV-1 genomic region overlapping env at the SU/TM boundary. Asp is found in pandemic strains of group M, but not in other primate lentiviruses including non-pandemic HIV-1 groups N, O, and P. We showed that asp is highly conserved despite constraining the evolution of env. We also reported that the asp gene is found at a higher frequency in people living with HIV-1 (PLWH) who progress to AIDS in <3 years (rapid progressors) compared to those who progress to AIDS in >12 years (long term non-progressors). The asp gene encodes the 189-aa hydrophobic protein, ASP. We reported that ASP shows high sequence iden- tity across HIV-1 isolates from all group-M subtypes. Work from our lab described the presence of ASP on the plasma membrane of infected cells, and on the envelope of infectious HIV-1 particles. Our unpublished studies demonstrate that the presence of ASP on the surface of HIV-1 particles facilitates viral entry. Several studies have shown the presence of cellular and humoral immune responses to ASP in PLWH, which proves its expression in vivo. A recent report reported that antibodies against ASP were specific for epitopes in the predicted ectodomain of ASP. Our preliminary studies confirmed the presence of antibodies against the ASP ectodomain in Elite Controllers (EC). Yet, none of the studies published so far endeavored to isolate ASP anti- bodies from PLWH and to test their functional activity as a way to investigate the role of ASP in HIV-1 infection. The overall aim of this application is to isolate monoclonal antibodies (mAbs) against the ectodomain of ASP from EC, Viremic Controllers, and PLWH both on and off ART. We will test their activity in in vitro and ex vivo assays. These studies will be performed in collaboration with Dr. Mohammad Sajadi (Institute of Human Virology, University of Maryland School of Medicine), who has established a cohort of >200 PLWH from whom he has already obtained paired serum and PBMC samples that are immediately available for the studies proposed here. Dr. Sajadi has developed a method for the identification, isolation, and cloning of mAbs that led to the discovery of best-in-class mAbs against HIV-1, SARS-CoV2, and CCHFV. Here, we propose the following specific aims: In Specific Aim 1, we will generate pools of overlapping peptides that span the ectodomain of ASP, and we will use these peptide pools to screen serum samples from PLWH in Dr. Sajadi’s cohort to identify those with strong- est binding to each of the five ASP peptide pools, and to determine their peptide sequence specificity. Next, we will use single-cell PCR and mass spectrometry to isolate and clone high affinity anti-ASP mAbs from the paired PBMC samples of the same donors. We will then validate the ASP specificity of these mAbs in ELISA and virion capture assays. In Specific Aim 2, we will test the activity of the ASP mAbs in mediating antibody dependent cellular toxicity (ADCC), reducing viral entry in single-round infection and viral replication in multiple rounds of infection, and detecting ASP on the cell surface, in the cytosol, and within nuclei.

Festa Italiana

The 32nd Annual Italian Festival will be held on September 28-29th from 10AM- 8PM at Seattle Center, 305 Harrison St. This community festival is designed to celebrate the arts and culture of Italy and those Americans of Italian descent. The celebration will features exhibits, music, dance, food and activities for the entire family.

NIAID - National Institute of Allergy and Infectious Diseases

People with HIV (PWH) on antiretroviral therapy (ART) experience persistent immune activation and inflammation despite effective viral suppression. Over time, this results in chronic inflammatory conditions across multiple organ systems, including neurocognitive decline and liver disease. The high risk for these conditions in PWH necessitates the identification of therapies to suppress inflammation that would be an adjunct to ART. One promising approach is through inhibition of the JAK-STAT signaling pathway. Small molecule JAK inhibitors (JAKi) have been highly successful in treating chronic inflammatory diseases and a second-generation orally available JAKi, baricitinib, is FDA approved for rheumatoid arthritis, alopecia areata, and systemic inflammation associated with COVID19. Recently, two Phase 2 clinical trials were initiated to evaluate the ability ofbaricitinib to control HIV replication and associated inflammation in PWH. like all clinical trials, these are limited in the types of samples that can be collected, resulting in a restriction to the mechanistic understanding of any viral or immune benefits that are observed. This proposal will bridge this gap by testing baricitinib in SN-infected macaques on ART (SIV +ARn, a system that is recognized as the gold standard for mechanistically evaluating HIV treatments. Our studies will test the hypothesis that JAK inhibition will reduce levels ofinflammatory biomarkers in tissues ofSN+ARTmacagues better than ART alone and that this benefit will be present even in a heightened inflammation model of/ow-dose lipopolysaccharide (LPS). We further hypothesize that reduced inflammation will result in lower SN levels and a smaller SN reservoir due to a reduction in activation and homeostatic proliferation of SN target cells. We will test the hypothesis in two specific aims, the first will assess peripheral tissues (blood and lymph nodes), while the second will assesses deep tissue sites within the macaques (CNS, lungs, liver and GI tract). Inflammatory mediators, immune cells and viral reservoirs will be assessed at each of these tissue sites. This proposal is timely as it investigates JAKi as potential anti-inflammatory and anti-viral therapy in the context of SIV +ART macaques, assessing key tissue sites that cannot be easily accessed during human clinical trials. In addition, baricitinib will be evaluated in the context of heightened inflammation associated with low-dose LPS exposure, with the potential to uncover strengths or weaknesses regarding JAK inhibition that might not be observed in a clinical trial. The long-term goal of the proposed studies is to obtain mechanistic insights into the effectiveness of JAK inhibition during SIV+ART. If proven efficacious, it is possible that baricitinib will be utilized as a therapy to suppress inflammation, reduce HIV replication, reduce HIV reservoir size, and increase life expectancy for PWH. We hope that the repurposing ofbaricitinib to address a persistent problem for PWH will represent a paradigm shift in the treatment of chronic HIV infection in the United States and globally.

Japantown Planning Group

The Japantown Planning Group (with fiscal sponsor Wing Luke Museum) requests funding for our Sakura Cherry Blossom Festival, in Seattle's Japantown, with weeklong activities April 7-12 culminating with main events on Saturday, April 13. Business owners and community members in Japantown have worked together over several years to activate Japantown businesses, streets, and parks and encourage more economic and pedestrian activity to help our recovery. Last year, we held the first Sakura Festival with an invitation to spend time in the neighborhood and enjoy music performances, art installations, food and business specials, walking tours, giveaways, a photo contest, and picnics in Kobe Terrace Park during cherry blossom time. Venues such as the Danny Woo and Chiyo?s Garden, Nihonmachi Alley, KOBO at Higo, Sairen, Panama Tea House, Wing Luke Museum, and more helped attract a diverse crowd in a successful event. We hope to build on that success as we welcome in Springtime together!

Jefferson

Jefferson Who Am I? is a theatrical performance based on the relationship between Thomas Jefferson our 5th president and his slave mistress Sally Hemings. The work will be presented on September 29th and 30th of 2018 at the Langston Hughes Center using several artistic disciplines including poetry, art, music and dance and performers of all ages. The project will stimulate healthy conversation on race and equity in American today, through facilitated discussions with the cast. All performances/events will be free and open to the public.

Central Area Chamber of Commerce

From 12pm - 6pm on Saturday June 15th and Sunday June 16th the Central Area Chamber of Commerce will host a celebration marking the emancipation of slavery. This year marks the 36th Juneteenth celebration at Pratt Park located at 1800 South Main Street and whose namesake, Edwin Pratt, was a trailblazer of the Civil Rights movement in Seattle. Juneteenth evokes the feeling of a family reunion, with event highlights including live music, spoken word, dance, art activities for kids, food, local small business vendors and community organizations. This year Juneteenth will also include a commemoration of the late DeCharlene Williams, the founder and long time leader of the Central Area Chamber of Commerce.

Kandelia

Kandelia's Culture Fair is an event to celebrate youth, families, diversity, and community across Seattle. Culture Fair will occur on June 3rd, 2023 from 9:30am - 1:30pm at Seattle World School (SWS). We are using SWS because it is an existing place of significance for our community and is central in the city for convenience. Culture Fair will celebrate newly arrived immigrant and refugee families. It will be a community event featuring food, music, dance, fashion, arts & crafts, sports, and people from diverse cultures. Attendees will be able to sample foods from different countries, participate in a friendly soccer game, and learn about different cultures. The event will also feature youth performances that include cultural dances, music performances, and fashion shows. Kandelia will invite immigrants and refugee families throughout Seattle. We will share the invite with our network of community partners, volunteers and the Central District neighborhood that surrounds SWS.

Kansas Creative Arts Industries Commission

The Kansas Creative Arts Industries Commission provides operating support grants to arts organizations across Kansas, funding programming, staffing, and capacity building that sustain the state's cultural infrastructure.

Kansas Creative Arts Industries Commission

Supports specific arts projects and programs across Kansas including festivals, exhibitions, performances, and community arts events that bring creative experiences to Kansas residents.

Kentucky Arts Council

Supports arts education programming in Kentucky schools and communities, funding artist residencies, arts integration professional development, and creative learning experiences for K-12 students.

Kentucky Arts Council

The Kentucky Arts Council provides operating support to Kentucky arts organizations for ongoing programming, operations, and capacity building that sustain arts and cultural experiences across the Commonwealth.

Kids and Paper

Starting in September of 2021, Kids and Paper plans to launch a new afterschool program to serve resettled children in grades K-5 with homework help, tutoring and healthy meals, along with programming that helps participants work on their social and emotional development through creative arts at the Magnuson Community Center located at 7110 62nd Ave NE Seattle, WA 98115. The anticipated project close out date is January 31, 2022.

One Vibe Africa

During the month of February, Kijiji Night 2020 will mark One Vibe Africa's 6th year partnering with the Seattle Art Museum to produce a free-to-the-public evening dedicated to celebrating the African Diaspora. On February 6, 2020, the spirit of an African village will be brought to life at SAM, 1300 1st Avenue from 5:00-9:00pm, through live hip-hop and traditional African musical performances, storytelling, poetry, and fresh food provided by Cafe Avole.

Friends of King Donut

A community mural will be installed at King Donuts, featuring four 6.5’ x 6’ wooden fence panels designed by a local artist. Each panel will be painted by Rainier Beach youth and community members using a color-by-number system, creating an inclusive and collaborative art piece. The mural’s design will be informed by a community event where local youth and residents contribute ideas and concept art. These events include art stations, food, and entertainment to support broad community participation and creative input. The anticipated project completion date is November 30, 2025.

Asian Americans for Arts Activism - A4A

Asian Americans for Arts Activism - A4A will host a free three-day celebration of Asian Pacific Islander American heritage month. The first event will be on May 26, 2018 from 11am - 1pm at Wing Luke Museum located at 719 S King St. The second will be on May 27, 2018 from 11am - 1pm at Seattle Public Library located at 1000 4th Ave. The final event will be on May 28, 2018 from 11am - 1pm at Royal Esquire Club located at 5016 Rainier Ave S. The events will feature workshops, film, art, and food.