Grants

LVMH Foundation

Funds environmental sustainability, biodiversity, and arts through luxury group philanthropy.

$25K – $1M

Environmentalbiodiversityarts

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LVMH-Arnault Foundation Grants

Arnault Foundation

Supports arts, culture, education, and community development through luxury industry philanthropy.

$25K – $1M

artscultureEducation

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LWCF Outdoor Recreation Legacy Partnership Program

Washington State Recreation and Conservation Office

Funding supports acquisition, development and renovation for public outdoor recreation and funds may be used for open space, forest, wildlife areas, beaches, and water access sites.

Free to search & build · $99 one-time to unlock the application pack · No subscription

LWCF Outdoor Recreation Legacy Partnership Program

Washington State Recreation and Conservation Office

Funding supports acquisition, development and renovation for public outdoor recreation and funds may be used for open space, forest, wildlife areas, beaches, and water access sites.

Free to search & build · $99 one-time to unlock the application pack · No subscription

LWCF Outdoor Recreation Legacy Partnership Program

Washington State Recreation and Conservation Office

Funding supports acquisition, development and renovation for public outdoor recreation and funds may be used for open space, forest, wildlife areas, beaches, and water access sites.

Free to search & build · $99 one-time to unlock the application pack · No subscription

LWCF Outdoor Recreation Legacy Partnership Program

Washington State Recreation and Conservation Office

Funding supports acquisition, development and renovation for public outdoor recreation and funds may be used for open space, forest, wildlife areas, beaches, and water access sites.

Free to search & build · $99 one-time to unlock the application pack · No subscription

LWCF Outdoor Recreation Legacy Partnership Program

Washington State Recreation and Conservation Office

Funding supports acquisition, development and renovation for public outdoor recreation and funds may be used for open space, forest, wildlife areas, beaches, and water access sites.

Free to search & build · $99 one-time to unlock the application pack · No subscription

LWCF Outdoor Recreation Legacy Partnership Program

Washington State Recreation and Conservation Office

Funding supports acquisition, development and renovation for public outdoor recreation and funds may be used for open space, forest, wildlife areas, beaches, and water access sites.

Free to search & build · $99 one-time to unlock the application pack · No subscription

LWCF Outdoor Recreation Legacy Partnership Program

Washington State Recreation and Conservation Office

Funding supports acquisition, development and renovation for public outdoor recreation and funds may be used for open space, forest, wildlife areas, beaches, and water access sites.

Free to search & build · $99 one-time to unlock the application pack · No subscription

Lymphatic Biology in Health and Disease (R01)

National Institutes of Health

Purpose. This Funding Opportunity Announcement (FOA) issued by the National Heart, Lung, and Blood Institute (NHLBI) solicits Research Project Grant (R01) applications from qualified researchers to investigate the biology of the lymphatic system and potential new therapeutic implications. The purpose of this program announcement is to stimulate research on the biology of the lymphatic system at all biologic levels: molecular, cellular, tissue, organ, and whole body levels. Further, it includes research on innovations for identifying and intervening in lymphatic diseases across all age groups and disease states. Mechanism of Support. This FOA will utilize the NIH Research Project Grant (R01) award mechanism. Funds Available and Anticipated Number of Awards. Awards issued under this FOA are contingent upon the availability of funds and the submission of a sufficient number of meritorious applications. Because the nature and scope of the proposed research will vary from application to application, it is anticipated that the size and duration of each award will also vary. The total amount awarded and the number of awards will depend upon the numbers, quality, duration, and costs of the applications received. Eligible Institutions/Organizations. Public/State Controlled Institution of Higher Education; Private Institution of Higher Education; Nonprofit with 501(c)(3) IRS Status (Other than Institution of Higher Education); Nonprofit without 501(c)(3) IRS Status (Other than Institution of Higher Education); Small Business; For-Profit Organization (Other than Small Business); State Government; U.S. Territory or Possession; Indian/Native American Tribal Government (Federally Recognized); Indian/Native American Tribal Government (Other than Federally Recognized); Indian/Native American Tribally Designated Organization; Non-domestic (non-U.S.) Entity (Foreign Organization); Hispanic-serving Institution; Historically Black Colleges and Universities (HBCUs); Tribally Controlled Colleges and Universities (TCCUs); Alaska Native and Native Hawaiian Serving Institutions; Regional Organization; Other(s); Eligible agencies of the Federal government; Faith-based or community based organizations. Eligible Project Directors/Principal Investigators (PDs/PIs). Individuals with the skills, knowledge, and resources necessary to carry out the proposed research are invited to work with their institution/organization to develop an application for support. Individuals from underrepresented racial and ethnic groups as well as individuals with disabilities are always encouraged to apply for NIH support. Number of Applications. Applicants may submit more than one application, provided each application is scientifically distinct. Renewals and Resubmissions. Applicants may submit a resubmission application, but such application must include an Introduction addressing the previous peer review critique (Summary Statement). Number of PDs/PIs. More than one PD/PI, or multiple PDs/PIs, may be designated on the application.

rolling

Education

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Lymphatic primary cilia regulation of intercellular junctions and valve formation

NHLBI - National Heart Lung and Blood Institute

Lymphatic valve dysfunction disrupts lymph transport, causing lymphedema – a condition characterized by irreversible tissue fibrosis and increased infection risk due to impaired immunosurveillance. Current standard of care manual lymph drainage and compression therapy fail to target the underlying molecular defects. This NIH R01 proposal builds on our discovery of the intraflagellar transport (IFT) system in lymphatic endothelial cells (LECs), focusing on IFT74 and IFT20 as critical regulators of lymphatic valve morphogenesis. IFT proteins, such as IFT74, are required for the assembly and maintenance of primary cilia, cell surface chemo- /mechanosignaling organelles that we recently discovered on LECs. IFT20 also performs essential non-ciliary processes, including trafficking adhesion and extracellular matrix (ECM) proteins. Our central hypothesis is that IFT proteins assemble primary cilia to promote shear stress-dependent lymphatic valve initiation and support valve maturation by non-ciliary trafficking of ECM and adhesion proteins to the cell surface to reinforce valve leaflets. Our preliminary data reveal that LEC-specific IFT74 knockout (KO) mice suffer defects in valve formation, while IFT20 KO mice show excessive lymphangiogenesis and impaired VE-cadherin recycling with more modest valve maturation defects, highlighting their distinct contributions. Specific Aim 1 will determine how IFT74/primary cilia enable lymphatic endothelial cells (LECs) to sense shear stress and initiate valve development. We will investigate ciliary signaling pathways using in vitro calcium flux assays, the role of transcriptional de-repression in valve morphogenesis, and identify valve-specific gene networks controlled by primary cilia via spatial transcriptomics. Specific Aim 2 will investigate how non-ciliary IFT20 regulates valve maturation by coordinating VE-cadherin recycling, integrin adhesion, and ECM deposition to stabilize valve leaflets. To determine how non-ciliary IFT20 exocytic trafficking promotes valve maturation, we will use intravital microscopy with transgenic reporters and second harmonic generation to observe valve formation and junctional/ECM dynamics in real time. We aim to elucidate the mechanisms of valve initiation and maturation, positioning IFT74/primary cilia and IFT20 and their downstream effectors as potential therapeutic targets for lymphedema. By connecting ciliary mechanosensation to valve development and non-ciliary trafficking to valve stability, we will build a comprehensive molecular model of IFT regulation of valve morphogenesis. Aligned with the NIH NOSI on the lymphatic system, this research seeks to enhance lymphatic transport capacity and guide the development of new therapies for lymphatic disorders.

Up to $453K

2031-01-31

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Lymphotoxin-dependent control of long COVID

NIAID - National Institute of Allergy and Infectious Diseases

SARS-CoV-2 infection causes acute lung pathology and can lead to long-term complications, collectively known as long COVID. These complications include persistent pain, headaches, myalgia, and post-exertional malaise. However, the mechanisms behind these neurological symptoms remain poorly understood. In particular, the role of sensory neurons in the pathogenesis of long COVID is largely unexplored. This knowledge gap hinders the development of novel therapeutic strategies for managing neurological complications associated with long COVID. Animal models are essential for investigating the role of sensory neurons in SARS-CoV-2 infection and testing preclinical interventions. Unfortunately, existing mouse models that allow for the study of SARS-CoV-2 specific effects on sensory neurons in vivo are lacking. In our research, we found that wild-type mice infected with a mouse- adapted SARS-CoV-2 strain develop long-term pain. To further explore the role of sensory neurons in long COVID, we developed a mouse model with selective SARS-CoV-2 infection of sensory neurons through hACE2 expression in Nav1.8+ neurons. Additionally, we identified lymphotoxin beta receptor (LTβR) as a novel immune regulator of chronic pain following SARS-CoV-2 infection. The objective of this proposal is to investigate the role of LTβR signaling in sensory neurons in the pathogenesis of long COVID and to test the potential of LTβR antagonist to mitigate neurological complications of long COVID. Our central hypothesis is that LTβR signaling in sensory neurons promotes long COVID neurological symptoms which can be ameliorated by administration of LTβR antagonist. This hypothesis will be tested through two specific aims. In Aim 1, we will define the impact of LTβR signaling in sensory neurons on long COVID neurological symptoms, viral replication, and immune cell changes in sensory ganglia, using mice with selective LTβR inactivation in Nav1.8+ sensory neurons. In Aim 2, we will assess the therapeutic effects of LTβR antagonist in alleviating long COVID neurological symptoms and identify critical LTβR-dependent pathways in sensory ganglia using single-cell RNA sequencing. This proposal is innovative, significant and impactful, as it will elucidate the role of sensory neurons in long COVID pain, establish new animal models for studying long COVID, and evaluate the therapeutic potential of LTβR antagonists for treating SARS-CoV-2-induced neurological complications.

Up to $235K

2028-01-31

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Lympnoids tissue senescence and multimodal imaging using REDCAT

NIA - National Institute on Aging

SUMMARY Cellular senescence, a hallmark of aging, is an irreversible state of cell cycle arrest in otherwise proliferative cells. Senescence in immune organs is particularly significant in aging and disease, as immune cells circulate throughout the body and regulate the physiological functions of all major organs. Metabolic alterations play a crucial role in immunosenescence and are recognized as key mechanisms driving abnormal immune homeostasis. To better understand the distinct role of senescent cell metabolism – for example, in thymic aging and immune function – there is a pressing need for novel methods to map senescent cells and cell-type-specific metabolism within complex tissues to assess their impact on the local environment. Given the critical role of immune senescence in systemic, organism-level aging, we hypothesize that: (i) thymic epithelial cell (TEC) senescence plays a key role in driving thymic aging. (ii) abnormal metabolic dynamics, including lipid metabolism and accumulated adipocytes in aged thymi, contribute to reduced T-cell diversity, (iii) senescence and aging in the thymus lead to systemic immune function decline. To address these hypotheses, we propose to develop and deploy an integrated platform, Raman Enhanced Determination of Cell Atlas and Typing (REDCAT), for mapping single-cell metabolic activity in complex tissues and decoding the underlying transcriptional and epigenomic mechanisms. It will be applied to the study of thymic aging in wild-type, lineage-tracked, and FGF21 mouse models. Specifically, we will (1) develop REDCAT for single-cell resolution profiling of cellular senescence in complex lymphoid tissues, (2) examine senescence-associated transcriptomic mechanisms via integrating DBiT- Based spatial transcriptome sequencing, and (3) investigating dynamic phenotypic and metabolomic heterogeneity of senescent cells in thymic aging and the impact on tissue microenvironments and systemic immune function. The proposed techniques can be widely adopted by the cellular senescence and aging research community. This work will also generate a valuable data resource to unveil insights in thymic aging to advance fundamental understanding of immuno-senescence and propel translational developments in anti- senescence interventions aimed at improving immune function and overall healthspan.

Up to $701K

2031-01-31

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Lysine Methylation as a Novel Regulatory Mechanism of HPV E2 Function

NIAID - National Institute of Allergy and Infectious Diseases

PROJECT ABSTRACT Human papillomaviruses (HPV) are double-stranded DNA viruses that infect cutaneous and mucosal epithelia. Infections with high-risk HPVs may lead to cervical, anogenital, and oropharyngeal cancers accounting for 5% of all cancers worldwide. Currently there are no effective non-invasive treatments against high-risk HPV infections. Because of that, it is critical to study the fundamental biology of high-risk HPV and specifically its utilization of host cell factors to permit completion of its viral life cycle. The viral replicative program consists of three different stages: (1) initial replication after infection, (2) stable maintenance of viral genomes and (3) amplification of viral episomes. The PV activator E2 and E1 DNA helicase proteins are the first proteins to be expressed after infection and are essential for HPV replication. The viral E2 protein is necessary for replication of the viral genome, activation of the viral early promoter for transcription, and tethering of viral genomes to host mitotic chromosomes in basal cells during cellular replication and division. Our long-term goal is to elucidate host factors necessary for E1-E2 dependent HPV replication and E2-mediated transcription throughout the viral lifecycle. Protein lysine methylation is emerging as an important post-translational modification that regulates the activity of transcription factors and histones. We recently identified four lysine residues methylated within the HPV-31 E2 by mass spectrometry confirming that E2 is a methylated protein. We hypothesize that that lysine methylation is an important regulatory process during the viral lifecycle. The overall objectives in this application are to (i) identify the lysine methyl transferases responsible for E2 methylation and (ii) determine their biological function. The proposed research is significant because it will define the mechanisms tightly controlled by E2 methylation throughout the HPV lifecycle. Ultimately, such knowledge has the potential to target mechanisms of persistent HPV infections.

Up to $209K

2028-04-30

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Lysine myristoylation as a novel mechanism for regulating PKA in the heart

NHLBI - National Heart Lung and Blood Institute

ABSTRACT Cardiovascular disease is a leading cause of death, with an uptick in cardiovascular disease mortality rates in recent years, due in part to the growing obesity crisis. Obesity is associated with many cardiovascular risk factors and increased adiposity can lead to cardiac remodeling and heart failure. One strategy to increase weight loss and improve cardiovascular outcomes is to target beta-adrenergic receptors (β-ARs) in adipose tissue to increase activation of protein kinase A (PKA) and increase energy expenditure. PKA also has important regulatory roles in cardiac tissue. PKA activation increases calcium cycling and contractility in the cardiomyocyte, thus increasing heart function. β-AR agonists, however, were not beneficial for long-term use in heart failure patients. We therefore need alternative mechanisms to activate and regulate PKA in the heart. We recently published that inhibiting histone deacetylase 11 (HDAC11) in adipocytes increased PKA activity and improved metabolic health. HDAC11 does not act like a classic HDAC, but rather, regulates protein function through lysine demyristoylation. Lysine demyristoylation is an understudied post-translational modification, and the biological functional consequences of lysine myristoylation/demyristoylation remain mostly unknown. Our preliminary data demonstrate that inhibition of HDAC11 increases the phosphorylation of PKA substrates in the cardiomyocytes. Our central hypothesis is that increasing lysine myristoylation in the cardiomyocyte (facilitated by HDAC11 inhibition) will beneficially increase heart function by increasing PKA activity. Aim 1 will determine the mechanism of HDAC11 inhibition-mediated increase in PKA activation by quantifying the myristoylation of the A kinase anchoring protein, gravin-α, which is known to facilitate HDAC11 inhibition-mediated PKA activation in adipocytes, through myristoyl-tag click chemistry and gain- and loss-of-function assays. We will also look for novel HDAC11 demyristoylation targets in the cardiomyocyte using click chemistry and mass spectrometry. Aim 2 will determine the functional effects of HDAC11 inhibition in the cardiomyocyte. We will evaluate the effect of HDAC11 inhibition at the cellular level by measuring calcium transients and function in isolated cardiomyocytes. We will generate a novel, inducible, cardiomyocyte-specific HDAC11 knockout mouse and assess cardiac structure and function in vivo using echocardiography, pressure-volume loop hemodynamics, and histological approaches. Finally, we will determine the functional effect of HDAC11 inhibition-mediated increase in PKA activation on disease pathogenesis and measure cardiac structure and function of wild-type and HDAC11 cardiomyocyte specific knockout mice before and after transverse aortic constriction. Together, successful completion of these aims will support the development of HDAC11 inhibitors as a novel therapeutic mechanism to regulate PKA activation and beneficially increase heart function.

Up to $75K

2028-12-31

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Lysosome-Golgi Contact Sites as Regulators of Senescence-Associated Inflammation

NIA - National Institute on Aging

PROJECT SUMMARY / ABSTRACT Chronic, low-grade inflammation is a hallmark of aging and a key driver of multiple age-related diseases. Accumulated senescent cells in aged tissues contribute to local and systemic inflammation by releasing a range of pro-inflammatory factors, collectively termed the senescence-associated secretory phenotype (SASP). Accordingly, there is growing interest in developing pharmacologic strategies to eliminate senescent cells and promote healthy aging. While senolytic drugs show promise, their off-target effects and dose-limiting toxicities constrain clinical use. An emerging alternative is the development of senomorphic therapies that suppress the SASP without inducing senescent cell clearance. However, progress has been hampered by an incomplete understanding of the regulatory mechanisms—particularly persistent NF-κB activation—that sustain SASP expression. Our recent work has uncovered a novel, spatially encoded mechanism underlying chronic inflammatory signaling in senescent cells. We identified a previously unrecognized class of lysosome–Golgi membrane contact sites (LG-MCSs) that form de novo during senescence and appear to act as structural scaffolds for the STING signalosome—a complex comprising the adaptor STING and the kinases TBK1 and IKKε, which together activate NF-κB. Unlike in canonical immune signaling, where STING is rapidly degraded via lysosomal routing after activation, we propose that senescent cells reorganize their organelle architecture to stabilize STING at LG-MCSs, shielding it from degradation and maintaining persistent signalosome activity. This R21 project will define the molecular architecture and functional role of LG-MCSs in sustaining chronic STING– NF-κB signaling. In Aim 1, we will use split-TurboID proximity labeling and quantitative mass spectrometry to generate a proteomic blueprint of LG-MCSs in senescent cells, identifying key tethering and signaling proteins. In Aim 2, we will employ CRISPR-based gene editing and the light-inducible OptoPBer system to manipulate LG-MCS formation in live cells and assess downstream effects on STING localization, NF-κB activation, and SASP gene expression. In addition to in vitro models of replicative and oncogene-induced senescence in normal human fibroblasts and epithelial cells, we will validate key findings in primary cells from aged donors and from individuals with Hutchinson-Gilford Progeria and Werner Syndromes—capturing both physiological and pathological contexts of aging. By establishing a new spatial framework for chronic inflammatory signaling in senescence, this project will generate foundational proof-of-concept data for a novel class of organelle-targeted senomorphic therapies. Aligned with the high-risk, high-reward mission of the R21 mechanism, these studies will lay the groundwork for future R01 research programs aimed at mitigating age-associated inflammation and promoting healthy aging through next-generation, organelle-based interventions.

Up to $429K

2028-04-30

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M--Boardwalk Replacement @ CUVA

INTERIOR, DEPARTMENT OF THE.NATIONAL PARK SERVICE.MWR OHIO(64000)

M--Boardwalk Replacement @ CUVA

general

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M--Railroad Tie Replacement

INTERIOR, DEPARTMENT OF THE.NATIONAL PARK SERVICE.MWR OHIO(64000)

M--Railroad Tie Replacement

general

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M.J. Murdock Charitable Trust Faith-Based Grants

M.J. Murdock Charitable Trust

Supports faith-based organizations, education, and scientific research in the Pacific Northwest (OR, WA, ID, MT, AK). One of the largest NW foundations.

$25K – $500K

Educationfaith-based organizationsscientific research

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M&E Toolkit: OCFT Sector-Specific Interventions and Cross-Cutting Themes

Bureau of International Labor Affairs

NOTE: This is a Notice of Intent. There is not an announcement related to this notice. We are not accepting applications at this time. Subject to the availability of funds, USDOL s Bureau of International Labor Affairs (ILAB) intends to award, through a competitive process, one or more cooperative agreements to organizations to implement a monitoring and evaluation project(s). The objective of the project is to develop an M&E toolkit for the Office of Child Labor, Forced Labor, and Human Trafficking (OCFT) and their grantees. This project will help build the capacity of OCFT s monitoring and evaluation efforts to better measure, target, monitor, and evaluate a growing portfolio of interventions. Specific sectors and cross-cutting themes to be addressed through the project are: occupational safety and health, forced labor, youth employment, labor-related technical and institutional capacity-building, gender and diversity, persons with disabilities, and migration. The M&E project will address these gaps through four mutually supporting outputs: 1) assessment and research on existing methods and indicators for monitoring and evaluation in the specified OCFT project sectors and cross-cutting themes; 2) development of tools, templates, and guidelines for each sector and cross-cutting theme; 3) development of guidelines and tools for end-of-project CMEP data analysis and identification of lessons learned in the identified sectors and themes; and 4) development and implementation of a dissemination and utilization strategy for the toolkit for both OCFT staff and grantees. The Employment and Training Administration (ETA) s Office of Grants Management anticipates publishing the Funding Opportunity Announcement (FOA) before the end of September 2016 (this date is subject to change). Please refer to: http://www.dol.gov/ilab/grants/ and http://www.dol.gov/ilab/grants/SGAguidelines.htm for general guidelines and examples of previous cooperative agreement applications. This NOI does not include an FOA or any attachments. It only constitutes a notice of USDOL s intent to publish an FOA at a later date. Interested applicants are encouraged to monitor www.grants.gov for the FOA because this is the method by which the FOA will be made available to the public. No email or paper copies of the FOA will be provided.

$1M

rolling

other

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M&T Bank Charitable Foundation

M&T Bank Foundation

Supports community revitalization, workforce development, and arts in the Northeast and Mid-Atlantic.

$5K – $250K

community developmentworkforce developmentarts

Free to search & build · $99 one-time to unlock the application pack · No subscription

MA Agriculture Grants

MA Dept of Agricultural Resources

Grants for farmland viability, specialty crops, and agricultural preservation.

$5K – $250K

Agriculture

Free to search & build · $99 one-time to unlock the application pack · No subscription

MA DEP Environmental Grants

MA Dept of Environmental Protection

Grants for clean water, waste reduction, and site cleanup programs in Massachusetts.

$10K – $500K

environmentwater_quality

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MA Executive Office of Housing and Livable Communities Community Development Action Grants

Massachusetts Executive Office of Housing and Livable Communities

The Community Development Action Grant (CDAG) program supports community development and housing activities in Massachusetts, funding infrastructure improvements, affordable housing development, and neighborhood revitalization.

$100K – $1M