Neural and mammary gland defects in ErbB4 knockout mice genetically rescued from embryonic lethality

Tidcombe, Hester; Jackson-Fisher, Amy; Mathers, Kathleen; Stern, David F.; Gassmann, Martin; Golding, Jon P.

doi:10.1073/pnas.1436402100

Cited by 238 publications

(299 citation statements)

References 41 publications

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“…As a consequence, these cells are capable of integrating environmental developmental signals far oV the immediate vicinity of their Wnal mitosis, in areas they reach only after protracted translocation. The observation that mice null for the ErbB4 receptor have increased numbers of large granule cell layer inhibitory interneurons suggests a role for the ErbB4/neuregulin signaling pathway in this scenario (Tidcombe et al 2003). Further, in vitro observations support the notion that such local cues include electrical activity and BDNF, which have been noted to regulate the expression of mGluR2 and parvalbumin, and also dendritic morphogenesis of cerebellar interneurons (Koscheck et al 2003;Mertz et al 2000).…”

Section: Development and Diverentiation Of Cerebellar (Cortical) Inhimentioning

confidence: 77%

Besides Purkinje cells and granule neurons: an appraisal of the cell biology of the interneurons of the cerebellar cortex

Schilling

Oberdick

Rossi

et al. 2008

Histochem Cell Biol

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Ever since the groundbreaking work of Ramon y Cajal, the cerebellar cortex has been recognized as one of the most regularly structured and wired parts of the brain formed by a rather limited set of distinct cells. Its rather protracted course of development, which persists well into postnatal life, the availability of multiple natural mutants, and, more recently, the availability of distinct molecular genetic tools to identify and manipulate discrete cell types have suggested the cerebellar cortex as an excellent model to understand the formation and working of the central nervous system. However, the formulation of a unifying model of cerebellar function has so far proven to be a most cantankerous problem, not least because our understanding of the internal cerebellar cortical circuitry is clearly spotty. Recent research has highlighted the fact that cerebellar cortical interneurons are a quite more diverse and heterogeneous class of cells than generally appreciated, and have provided novel insights into the mechanisms that underpin the development and histogenetic integration of these cells. Here, we provide a short overview of cerebellar cortical interneuron diversity, and we summarize some recent results that are hoped to provide a primer on current understanding of cerebellar biology.

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Section: Development and Diverentiation Of Cerebellar (Cortical) Inhimentioning

confidence: 77%

Besides Purkinje cells and granule neurons: an appraisal of the cell biology of the interneurons of the cerebellar cortex

Schilling

Oberdick

Rossi

et al. 2008

Histochem Cell Biol

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“…One of the primary functions of ErbB4 in vivo is in the maturation of mammary glands during pregnancy and WWP1 targets ErbB4 for degradation Y Li et al lactation induction (Long et al, 2003;Tidcombe et al, 2003). ErbB4 can activate the expression of the tumor suppressor gene, BRCA1, (Muraoka-Cook et al, 2006a) and differentiation genes such as b-casein (Muraoka-Cook et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

WW domain containing E3 ubiquitin protein ligase 1 targets the full-length ErbB4 for ubiquitin-mediated degradation in breast cancer

Zhou

Alimandi

et al. 2009

Oncogene

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ErbB4, a member of the epidermal growth factor receptor family, plays a role in normal breast and breast cancer development by regulating mammary epithelial cell proliferation, survival and differentiation. In this study, we show that WWP1, a C2-WW-HECT type E3 ubiquitin ligase, binds, ubiquitinates and destructs ErbB4-CYT1, but much less efficiently for CYT2, isoforms (both JMa and JMb). The protein-protein interaction occurs primarily between the first and third WW domains of WWP1 and the second PY motif of ErbB4. Knockdown of WWP1 by two different small interfering RNAs increases the endogenous ErbB4 protein levels in both MCF7 and T47D breast cancer cell lines. In addition, overexpression of the wild type, but not the catalytic inactive WWP1, dramatically decreases the endogenous ErbB4 protein levels in MCF7. Importantly, we found that WWP1 negatively regulates the heregulin-b1-stimulated ErbB4 activity as measured by the serum response element report assay and the BRCA1 mRNA expression. After a systematic screening of all WWP1 family members by small interfering RNA, we found that AIP4/Itch and HECW1/NEDL1 also negatively regulate the ErbB4 protein expression in T47D. Interestingly, the protein expression levels of both WWP1 and ErbB4 are higher in estrogen receptor-a-positive than in estrogen receptor-anegative breast cancer cell lines. These data suggest that WWP1 and its family members suppress the ErbB4 expression and function in breast cancer.

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“…ErbB4 is essential for cardiac development. The embryonic lethality associated with constitutional disruption of ErbB4 can be bypassed by expression of a human HER4 cDNA in the heart under control of a mouse a-myosin heavy chain promoter (Tidcombe et al, 2003). ErbB4 À/À animals carrying this HER4 heart transgene reach adulthood and are fertile, but have cranial nerve and cerebellar defects, and impaired mammary differentiation and lactation.…”

Section: Resultsmentioning

confidence: 99%

“…The floxed ErbB4 and ErbB4 null mice were backcrossed into FVB background for a minimum of seven generations before breeding to generate mice for analysis. Conditional knock-out HER4 heart ErbB4 À/À mice (Tidcombe et al, 2003) were obtained from Dr Martin Gassmann. All animal experiments were performed under a Yale University Institutional Animal Care and Use Committee approved protocol.…”

Section: Methodsmentioning

confidence: 99%

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Formation of Neu/ErbB2-induced mammary tumors is unaffected by loss of ErbB4

et al. 2006

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The four members of the ErbB family of receptor tyrosine kinases are involved in development and tumorigenesis of the mammary gland. Whereas the epidermal growth factor receptor, ErbB2 and ErbB3 are positively associated with various cancers, clinical studies of ErbB4 in breast cancer are contradictory. Results from tissue culture analyses and some clinical studies suggested that ErbB4 is either a tumor suppressor or is a negative regulator of ErbB2-driven tumors. Neu-Cre-ErbB4 flox/null mice in which ErbB4 was inactivated by Cre-lox-mediated recombination in the mammary gland developed MMTVNeu-driven mammary tumors with a similar latency period to mice with one or two wild-type ErbB4 alleles. Moreover, there was no difference in the histologies of tumors that developed, nor in the propensity to form lung metastases. Taken together these results suggest that ErbB4 is not a potent, highly penetrant tumor suppressor, nor is it a factor in Neu-mediated tumorigenesis in this model.

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Neural and mammary gland defects in ErbB4 knockout mice genetically rescued from embryonic lethality

Cited by 238 publications

References 41 publications

Besides Purkinje cells and granule neurons: an appraisal of the cell biology of the interneurons of the cerebellar cortex

Besides Purkinje cells and granule neurons: an appraisal of the cell biology of the interneurons of the cerebellar cortex

WW domain containing E3 ubiquitin protein ligase 1 targets the full-length ErbB4 for ubiquitin-mediated degradation in breast cancer

Formation of Neu/ErbB2-induced mammary tumors is unaffected by loss of ErbB4

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