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hpa010687

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Bok regulates mitochondrial fusion and morphology.

Jacqualyn J Schulman et al.

Cell death and differentiation, 26(12), 2682-2694 (2019-04-13)

Bok (Bcl-2-related ovarian killer) is a member of the Bcl-2 protein family that governs the intrinsic apoptosis pathway, but the cellular role that Bok plays is controversial. Remarkably, endogenous Bok is constitutively bound to inositol 1,4,5-trisphosphate receptors (IP3Rs) and is

DISC1-dependent Regulation of Mitochondrial Dynamics Controls the Morphogenesis of Complex Neuronal Dendrites.

Rosalind Norkett et al.

The Journal of biological chemistry, 291(2), 613-629 (2015-11-11)

The DISC1 protein is implicated in major mental illnesses including schizophrenia, depression, bipolar disorder, and autism. Aberrant mitochondrial dynamics are also associated with major mental illness. DISC1 plays a role in mitochondrial transport in neuronal axons, but its effects in

Atypical Rho GTPases have roles in mitochondrial homeostasis and apoptosis.

Asa Fransson et al.

The Journal of biological chemistry, 278(8), 6495-6502 (2002-12-17)

The human genomic sequencing effort has revealed the presence of a large number of Rho GTPases encoded by the human genome. Here we report the characterization of a new family of Rho GTPases with atypical features. These proteins, which were

Molecular markers implicating early malignant events in cervical carcinogenesis.

Hanna-Mari Koskimaa et al.

Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 19(8), 2003-2012 (2010-07-22)

Human papillomavirus can induce a stepwise progression of precursor lesions to carcinoma. Sensitive and specific molecular markers are needed to identify the cervical lesions (CIN) at risk for this progression. hTERT activation could be one indicator of a point of

Immunofluorescence and fluorescent-protein tagging show high correlation for protein localization in mammalian cells.

Charlotte Stadler et al.

Nature methods, 10(4), 315-323 (2013-02-26)

Imaging techniques such as immunofluorescence (IF) and the expression of fluorescent protein (FP) fusions are widely used to investigate the subcellular distribution of proteins. Here we report a systematic analysis of >500 human proteins comparing the localizations obtained in live

Miro1 Regulates Activity-Driven Positioning of Mitochondria within Astrocytic Processes Apposed to Synapses to Regulate Intracellular Calcium Signaling.

Terri-Leigh Stephen et al.

The Journal of neuroscience : the official journal of the Society for Neuroscience, 35(48), 15996-16011 (2015-12-04)

It is fast emerging that maintaining mitochondrial function is important for regulating astrocyte function, although the specific mechanisms that govern astrocyte mitochondrial trafficking and positioning remain poorly understood. The mitochondrial Rho-GTPase 1 protein (Miro1) regulates mitochondrial trafficking and detachment from

VAPB interacts with the mitochondrial protein PTPIP51 to regulate calcium homeostasis.

Kurt J De Vos et al.

Human molecular genetics, 21(6), 1299-1311 (2011-12-02)

A proline to serine substitution at position 56 in the gene encoding vesicle-associated membrane protein-associated protein B (VAPB) causes some dominantly inherited familial forms of motor neuron disease including amyotrophic lateral sclerosis (ALS) type-8. VAPB is an integral endoplasmic reticulum

Mfn2 ubiquitination by PINK1/parkin gates the p97-dependent release of ER from mitochondria to drive mitophagy.

Gian-Luca McLelland et al.

eLife, 7 (2018-04-21)

Despite their importance as signaling hubs, the function of mitochondria-ER contact sites in mitochondrial quality control pathways remains unexplored. Here we describe a mechanism by which Mfn2, a mitochondria-ER tether, gates the autophagic turnover of mitochondria by PINK1 and parkin.

The mitochondrial deubiquitinase USP30 opposes parkin-mediated mitophagy.

Baris Bingol et al.

Nature, 510(7505), 370-375 (2014-06-05)

Cells maintain healthy mitochondria by degrading damaged mitochondria through mitophagy; defective mitophagy is linked to Parkinson's disease. Here we report that USP30, a deubiquitinase localized to mitochondria, antagonizes mitophagy driven by the ubiquitin ligase parkin (also known as PARK2) and

The atypical Rho GTPases Miro-1 and Miro-2 have essential roles in mitochondrial trafficking.

Sa Fransson et al.

Biochemical and biophysical research communications, 344(2), 500-510 (2006-04-25)

We recently described the atypical Rho GTPases Miro-1 and Miro-2. These proteins have tandem GTP-binding domains separated by a linker region with putative calcium-binding motives. In addition, the Miro GTPases have a C-terminal transmembrane domain, which confers targeting to the

Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits.

Bing Zhou et al.

The Journal of cell biology, 214(1), 103-119 (2016-06-09)

Although neuronal regeneration is a highly energy-demanding process, axonal mitochondrial transport progressively declines with maturation. Mature neurons typically fail to regenerate after injury, thus raising a fundamental question as to whether mitochondrial transport is necessary to meet enhanced metabolic requirements

Mitotic redistribution of the mitochondrial network by Miro and Cenp-F.

Gil Kanfer et al.

Nature communications, 6, 8015-8015 (2015-08-12)

Although chromosome partitioning during mitosis is well studied, the molecular mechanisms that allow proper segregation of cytoplasmic organelles in human cells are poorly understood. Here we show that mitochondria interact with growing microtubule tips and are transported towards the daughter

Lysine 27 ubiquitination of the mitochondrial transport protein Miro is dependent on serine 65 of the Parkin ubiquitin ligase.

Nicol Birsa et al.

The Journal of biological chemistry, 289(21), 14569-14582 (2014-03-29)

Mitochondrial transport plays an important role in matching mitochondrial distribution to localized energy production and calcium buffering requirements. Here, we demonstrate that Miro1, an outer mitochondrial membrane (OMM) protein crucial for the regulation of mitochondrial trafficking and distribution, is a

Alpha-synuclein delays mitophagy and targeting Miro rescues neuron loss in Parkinson's models.

Atossa Shaltouki et al.

Acta neuropathologica, 136(4), 607-620 (2018-06-21)

Alpha-synuclein is a component of Lewy bodies, the pathological hallmark of Parkinson's disease (PD), and is also mutated in familial PD. Here, by extensively analyzing PD patient brains and neurons, and fly models, we show that alpha-synuclein accumulation results in

APC binds the Miro/Milton motor complex to stimulate transport of mitochondria to the plasma membrane.

Kate M Mills et al.

Molecular biology of the cell, 27(3), 466-482 (2015-12-15)

Mutations in adenomatous polyposis coli (APC) disrupt regulation of Wnt signaling, mitosis, and the cytoskeleton. We describe a new role for APC in the transport of mitochondria. Silencing of wild-type APC by small interfering RNA caused mitochondria to redistribute from

Principles of the mitochondrial fusion and fission cycle in neurons.

Michal Cagalinec et al.

Journal of cell science, 126(Pt 10), 2187-2197 (2013-03-26)

Mitochondrial fusion-fission dynamics play a crucial role in many important cell processes. These dynamics control mitochondrial morphology, which in turn influences several important mitochondrial properties including mitochondrial bioenergetics and quality control, and they appear to be affected in several neurodegenerative

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