The role of the receptor complex and the cofactors in IGSF10 signaling
The role of the receptor complex and the cofactors in IGSF10 signaling
批准号:
10728450
负责人:
YUZURU SHIIO
金额:
$35.46万
依托单位国家:
美国
项目类别:
财政年份:
2023
资助国家:
美国
项目状态:
未结题
起止时间:
2023-06-07 至 2028-05-31
关键词:
Basic ScienceBindingBiologicalBiological ProcessBiologyC-terminalCell LineCell ProliferationCell Surface ProteinsCell Surface ReceptorsCell modelCellsCleidocranial DysplasiaCollaborationsComplexCysteine-Rich DomainDelayed PubertyEwings sarcomaFoundationsFrameshift MutationFutureGene ExpressionGliomaGonadotropin Hormone Releasing HormoneGrowthHumanImmunoglobulinsInheritedKnowledgeLeucine-Rich RepeatLigandsLinkMalignant neoplasm of lungMediatingMicrogliaMolecularMusMutationN-terminalNational Institute of Neurological Disorders and StrokeNeuronsPathologicPathologic ProcessesPathway interactionsPhenocopyPhysiologicalPituitary HormonesPlayProtein SecretionProtein Tyrosine KinaseProteomicsRET inhibitionResearchRoleSignal PathwaySignal TransductionStructureSystemTestingTherapeuticTissuesUnited States National Institutes of HealthVariantcofactorhormone deficiencyimmunoglobulin receptorinhibitorkinase inhibitorknock-downmalignant breast neoplasmmembermigrationmutantnovelolfactomedinpreventprotein functionproto-oncogene protein c-retreceptorskeletal disordertranscriptome sequencingtumor
中文摘要
免疫球蛋白超家族成员10(IGSF10)是一种大的分泌性蛋白,参与多种生物学过程
病理过程:IGSF10突变与遗传性青春期延迟有关。低IGSF10
这种表达与更具侵袭性的肺癌和乳腺癌有关。IGSF10中发现移码突变
一例遗传性骨骼疾病,锁骨发育不良。在联合体中发现IGSF10 A1672T变异
脑垂体激素缺乏症。然而,IGSF10的作用机制尚不清楚。
申请人的团队确定了IGSF10的细胞表面受体和下游信号通路
受IGSF10监管。他们还确定了IGSF10的一个假定的辅助受体和一个分泌的辅助因子。这
该项目旨在了解受体复合体和辅助因子在IGSF10中的作用
发信号。该项目的成功完成将揭示其分子机制和生物学特性。
IGSF10介导的新信号通路的作用。从这个项目中获得的知识将为
为了解这一新的信号通路的生理作用以及病理机制奠定基础
与这一途径的失调相关的条件。
英文摘要
Immunoglobulin superfamily member 10 (IGSF10) is a large, secreted protein implicated in multiple biological
and pathological processes: IGSF10 mutations are associated with hereditary delayed puberty. Low IGSF10
expression is linked to more aggressive lung and breast cancers. A frameshift mutation in IGSF10 was found in
a case of a hereditary skeletal disorder, Cleidocranial Dysplasia. IGSF10 A1672T variant was found in combined
pituitary hormone deficiency. However, the mechanism of action of IGSF10 is unknown.
The applicant’s group identified the cell surface receptor for IGSF10 and the downstream signaling pathway
regulated by IGSF10. They also identified a putative co-receptor and a secreted co-factor for IGSF10. This
project is directed towards understanding the roles of the receptor complex and the cofactors in IGSF10
signaling. The successful completion of the project will uncover the molecular mechanisms and the biological
roles of the novel signaling pathway mediated by IGSF10. The knowledge gained from this project will lay the
foundation for understanding the physiological roles of this novel signaling pathway as well as the pathological
conditions associated with the dysregulation of this pathway.
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