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Last update 08 May 2025

ITGA9

Last update 08 May 2025

Basic Info

Synonyms

ALPHA-RLC, Integrin alpha-9, Integrin alpha-RLC

+ [6]

Introduction

Integrin alpha-9/beta-1 (ITGA9:ITGB1) is a receptor for VCAM1, cytotactin and osteopontin. It recognizes the sequence A-E-I-D-G-I-E-L in cytotactin. ITGA9:ITGB1 may play a crucial role in SVEP1/polydom-mediated myoblast cell adhesion (By similarity). Integrin ITGA9:ITGB1 represses PRKCA-mediated L-type voltage-gated channel Ca(2+) influx and ROCK-mediated calcium sensitivity in vascular smooth muscle cells via its interaction with SVEP1, thereby inhibiting vasocontraction (PubMed:35802072).

Drugs associated with ITGA9

GND-001

Target

ITGA9

Mechanism

ITGA9 antagonists

Active Org.

Kaken Pharmaceutical Co., Ltd. [+1]

Originator Org.

Kidswell Bio Corp.

Active Indication

Immune System Diseases [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

ASP-5094

Target

ITGA9

Mechanism

ITGA9 antagonists

Active Org.-

Originator Org.

Astellas Pharma, Inc.

Active Indication-

Inactive Indication

Rheumatoid Arthritis

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with ITGA9

NCT03257852

/ CompletedPhase 2

A Phase 2a, Randomized, Placebo-Controlled, Double-Blind, Parallel Group Study to Evaluate the Efficacy and Safety of ASP5094 in Patients With Rheumatoid Arthritis on Methotrexate

The objective of this study is to evaluate the efficacy, safety and pharmacokinetics of ASP5094 in patients with rheumatoid arthritis (RA) treated with background methotrexate (MTX).

Start Date29 Sep 2017

Sponsor / Collaborator

Astellas Pharma, Inc.

NCT02698657

/ CompletedPhase 1

A Phase 1, Randomized, Placebo-controlled, Dose Escalation Study to Assess the Safety, Tolerability, and Pharmacokinetics of ASP5094 Following Multiple Intravenous Doses in Subjects With Rheumatoid Arthritis on Methotrexate

The purpose of this study is to evaluate the safety, tolerability and pharmacokinetics of multiple ascending intravenous doses of ASP5094 in male and female subjects with rheumatoid arthritis (RA) on methotrexate (MTX).

Start Date23 Feb 2016

Sponsor / Collaborator

Astellas Pharma Global Development, Inc.

100 Clinical Results associated with ITGA9

100 Translational Medicine associated with ITGA9

0 Patents (Medical) associated with ITGA9

165

Literatures (Medical) associated with ITGA9

09 Apr 2025·The Journal of Neuroscience

The Medial Olivocochlear Efferent Pathway Potentiates Cochlear Amplification in Response to Hearing Loss

Article

Author: Wang, Juemei ; Quiñones, Patricia M ; Srivastava, Hemant ; Dewey, James B ; Serafino, Michael J ; Macias-Escriva, Frank ; Applegate, Brian E ; Oghalai, John S ; McGinley, Matthew J ; Kim, Bong Jik ; Cobo-Cuan, Ariadna ; Morán, Marcela A ; Walker, Clayton B ; Pei, Michelle

The mammalian cochlea receives efferent feedback from the brain. Many functions for this feedback have been hypothesized, including on short timescales, such as mediating attentional states, and long timescales, such as buffering acoustic trauma. Testing these hypotheses has been impeded by an inability to make direct measurements of efferent effects in awake animals. Here, we assessed the role of the medial olivocochlear (MOC) efferent nerve fibers on cochlear amplification by measuring organ of Corti vibratory responses to sound in both sexes of awake and anesthetized mice. We studied long-term effects by genetically ablating the efferents and/or afferents. Cochlear amplification increased with deafferentation using VGLUT3 −/− mice, but only when the efferents were intact, associated with increased activity within OHCs and supporting cells. Removing both the afferents and the efferents using VGLUT3 −/− Alpha9 −/− mice did not cause this effect. To test for short-term effects, we recorded sound-evoked vibrations while using pupillometry to measure neuromodulatory brain state. We found no state dependence of cochlear amplification or of the auditory brainstem response. However, state dependence was apparent in the downstream inferior colliculus. Thus, MOC efferents upregulate cochlear amplification chronically with hearing loss, but not acutely with brain state fluctuations. This pathway may partially compensate for hearing loss while mediating associated symptoms, such as tinnitus and hyperacusis.

01 Nov 2024·Gene

Integrin-α9 overexpression underlies the niche-independent maintenance of leukemia stem cells in acute myeloid leukemia

Article

Author: Niibori-Nambu, Akiko ; Tergaonkar, Vinay ; Chooi, Jing Yuan ; Wang, Chelsia Qiuxia ; Goh, Yufen ; Yang, Henry ; Osato, Motomi ; Taniuchi, Ichiro ; Tham, Cheng-Yong ; Fam, Wee Nih ; Sonoki, Takashi ; Fullwood, Melissa Jane ; Suda, Toshio ; Hosoi, Hiroki ; Tan, Darren Qiancheng ; Tng, Jiaqi ; Chng, Wee Joo ; Chin, Desmond Wai Loon ; Nah, Giselle Sek Suan ; Li, Shang ; Takizawa, Hitoshi ; Cirovic, Branko ; Sashida, Goro

Leukemia stem cells (LSCs) are widely believed to reside in well-characterized bone marrow (BM) niches; however, the capacity of the BM niches to accommodate LSCs is insufficient, and a significant proportion of LSCs are instead maintained in regions outside the BM. The molecular basis for this niche-independent behavior of LSCs remains elusive. Here, we show that integrin-α9 overexpression (ITGA9 OE) plays a pivotal role in the extramedullary maintenance of LSCs by molecularly mimicking the niche-interacting status, through the binding with its soluble ligand, osteopontin (OPN). Retroviral insertional mutagenesis conducted on leukemia-prone Runx-deficient mice identified Itga9 OE as a novel leukemogenic event. Itga9 OE activates Akt and p38MAPK signaling pathways. The elevated Myc expression subsequently enhances ribosomal biogenesis to overcome the cell integrity defect caused by the preexisting Runx alteration. The Itga9-Myc axis, originally discovered in mice, was further confirmed in multiple human acute myeloid leukemia (AML) subtypes, other than RUNX leukemias. In addition, ITGA9 was shown to be a functional LSC marker of the best prognostic value among 14 known LSC markers tested. Notably, the binding of ITGA9 with soluble OPN, a known negative regulator against HSC activation, induced LSC dormancy, while the disruption of ITGA9-soluble OPN interaction caused rapid cell propagation. These findings suggest that the ITGA9 OE increases both actively proliferating leukemia cells and dormant LSCs in a well-balanced manner, thereby maintaining LSCs. The ITGA9 OE would serve as a novel therapeutic target in AML.

01 Jun 2024·Regenerative Therapy

METTL3 promotes the osteogenic differentiation of periosteum-derived MSCs via regulation of the HOXD8/ITGA5 axis in congenital pseudarthrosis

Article

Author: Yan, An ; Liu, Yaoxi ; Tan, Qian ; Xiao, Han ; Ye, Weihua ; Zhu, Guanghui ; Liu, Zheng

BackgroundCongenital pseudarthrosis of the tibia (CPT) is a dominant health challenge in pediatric orthopedics. The essential process in the development of CPT is the limited capacity of mesenchymal stem cells (MSCs) derived from CPT to undergo osteogenic differentiation. Our research aimed to elucidate the role and mechanism of methyltransferase-like 3 (METTL3) in the osteogenic differentiation process of CPT MSCs.MethodsThe osteogenic differentiation medium was used to culture MSCs, and the detection of osteogenic differentiation was performed using Alizarin Red S and alkaline phosphatase (ALP) assays. Gene or protein expression was assessed by quantitative real-time polymerase chain reaction (qRT-PCR), Western blot, or immunofluorescence (IF) staining. The m⁶A modification of Homeobox D8 (HOXD8) was verified by methylated RNA immunoprecipitation (MeRIP) assay. Interactions between METTL3 and HOXD8 or HOXD8 and integrin alpha 5 (ITGA5) promoter were validated by the luciferase reporter gene, RIP, and chromatin immunoprecipitation (ChIP) assays.ResultsMETTL3 overexpression enhanced CPT MSCs' osteogenic differentiation. METTL3 stabilized the HOXD8 in an m⁶A-dependent manner. Moreover, the overexpressed ITGA5 up-regulated the CPT MSCs' osteogenic differentiation. Further, HOXD8 could transcriptionally activate ITGA5. METTL3 increased the transcription of ITGA5 via HOXD8 to enhance the osteogenic differentiation of CPT MSCs.ConclusionMETTL3 promoted osteogenic differentiation via modulating the HOXD8/ITGA5 axis in CPT MSCs.

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ITGA9

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